greenmedinfo--2020-08-08--Radiation-induced gastrointestinal syndrome is exacerbated in vitamin C-insufficient SMP30/GNL knock

Radiation-induced gastrointestinal syndrome is exacerbated in vitamin C-insufficient SMP30/GNL knockout mice.

OBJECTIVES : Accidental exposure to high-dose radiation causes life-threatening acute radiation syndrome , features that include gastrointestinal syndrome ( GIS ) and hematopoietic syndrome ( HS ) .
Administration of vitamin C ( VC ) , a free radical scavenger , has been reported to increase survival of mice in GIS and HS models .
The effect of nutritional VC status on radiation injury remains unknown because , unlike humans , mice can synthesize VC .
The aim of this study was to investigate the effect of VC insufficiency on acute radiation syndrome using senescence marker protein 30 ( SMP30 @ @ @ @ @ @ @ .
METHODS : SMP30-KO mice , which can not synthesize VC , were given water with or without sufficient VC supplementation , and were analyzed in GIS and HS models .
RESULTS : In the GIS model , in which bone marrow failure is rescued by bone marrow transplantation , VC-insufficient mice had a lower survival rate than VC-sufficient mice .
The intestine of VC-insufficient GIS mice showed epithelial cell atrophy , inflammatory cell infiltration , and decreased crypt cell proliferation .
We observed rapid VC oxidation after total body irradiation in the @ @ @ @ @ @ @ .
In the HS model , which was not combined with bone marrow transplantation , there was no difference in survival between VC-insufficient and -sufficient mice .
CONCLUSION : The results of this study demonstrated that nutritionally sufficient VC exerts a radioprotective effect against radiation-induced GIS .

OBJECTIVES: Accidental exposure to high-dose radiation causes life-threatening acute radiation syndrome, features that include gastrointestinal syndrome (GIS) and hematopoietic syndrome (HS). Administration of vitamin C (VC), a free radical scavenger, has been reported to increase survival of mice in GIS and HS models. The effect of nutritional VC status on radiation injury remains unknown because, unlike humans, mice can synthesize VC. The aim of this study was to investigate the effect of VC insufficiency on acute radiation syndrome using senescence marker protein 30 (SMP30)/gluconolactonase knockout (SMP30-KO) mice.
METHODS: SMP30-KO mice, which cannot synthesize VC, were given water with or without sufficient VC supplementation, and were analyzed in GIS and HS models.
RESULTS: In the GIS model, in which bone marrow failure is rescued by bone marrow transplantation, VC-insufficient mice had a lower survival rate than VC-sufficient mice. The intestine of VC-insufficient GIS mice showed epithelial cell atrophy, inflammatory cell infiltration, and decreased crypt cell proliferation. We observed rapid VC oxidation after total body irradiation in the intestine of mice supplemented with VC-sufficient water. In the HS model, which was not combined with bone marrow transplantation, there was no difference in survival between VC-insufficient and -sufficient mice.
CONCLUSION: The results of this study demonstrated that nutritionally sufficient VC exerts a radioprotective effect against radiation-induced GIS.


greenmedinfo--2020-08-08--Vitamins C and E have protective effects against preeclampsia by alleviating the overall blood press

Vitamins C and E have protective effects against preeclampsia by alleviating the overall blood pressure.

Objectives Preeclampsia is a hypertensive disorder associated with pregnancy and is the leading cause of both maternal and neonatal morbidity and mortality .
Recent reports suggest that free radical-induced endothelial cell injury might be an etiologic factor in the pathogenesis of preeclampsia .
The aim of this study was to determine the protective effects of vitamins C and E for the prevention of preeclampsia .
Methods This clinical trial was conducted in the year 2018 in the clinical centers of Lorestan University of Medical Sciences .
One hundred and sixty nulliparous women aged 18-38 years without any risk factors for @ @ @ @ @ @ @ The first group received a 400-IU/day dose of vitamin E orally and a 1000-mg/day dose of vitamin C with iron tablets during 20-24 weeks of pregnancy , while the control group received only iron tablets .
Finally , the data were analyzed using descriptive statistics and frequency distribution tables .
Results The incidence of preeclampsia in the control group was 17.5 % and in the intervention group was 5 % , which was significantly different .
The mean systolic pressures before and after intervention were 99.43 ± 7.8 and 12.44 ± 19.1 , @ @ @ @ @ @ @ and 99.3 ± 8.3 and 106.12 ± 13.25 , respectively , in the intervention group ( P

Objectives Preeclampsia is a hypertensive disorder associated with pregnancy and is the leading cause of both maternal and neonatal morbidity and mortality. Recent reports suggest that free radical-induced endothelial cell injury might be an etiologic factor in the pathogenesis of preeclampsia. The aim of this study was to determine the protective effects of vitamins C and E for the prevention of preeclampsia. Methods This clinical trial was conducted in the year 2018 in the clinical centers of Lorestan University of Medical Sciences. One hundred and sixty nulliparous women aged 18-38 years without any risk factors for preeclampsia were divided into two groups. The first group received a 400-IU/day dose of vitamin E orally and a 1000-mg/day dose of vitamin C with iron tablets during 20-24 weeks of pregnancy, while the control group received only iron tablets. Finally, the data were analyzed using descriptive statistics and frequency distribution tables. Results The incidence of preeclampsia in the control group was 17.5% and in the intervention group was 5%, which was significantly different. The mean systolic pressures before and after intervention were 99.43 ± 7.8 and 12.44 ± 19.1, respectively, in the control group, and 99.3 ± 8.3 and 106.12 ± 13.25, respectively, in the intervention group (P < 0.001). The mean diastolic pressures before and after intervention in the control group were 62.7 ± 13.6 and 62.7 ± 4.7 (P < 0.001), respectively. Conclusion The results of this study show that vitamins C and E have protective effects against preeclampsia by alleviating the overall blood pressure.


greenmedinfo--2020-08-08--Vitamin C deficiency: An under-recognized condition in Crohn's disease.

Although many nutritional deficiencies are associated with Crohn 's disease ( CD ) , vitamin C deficiency is less frequently @ @ @ @ @ prevalence .
Vitamin C deficiency may be more difficult to diagnose in patients with CD @ @ @ @ @ may overlap with scurvy .
Identification of the deficiency is vital , however , because @ @ @ @ @ , marked resolution of symptoms .
We present a patient with long-standing CD who presented @ @ @ @ @ found to have scurvy .

Although many nutritional deficiencies are associated with Crohn's disease (CD), vitamin C deficiency is less frequently diagnosed and reported despite its prevalence. Vitamin C deficiency may be more difficult to diagnose in patients with CD because symptoms from active CD may overlap with scurvy. Identification of the deficiency is vital, however, because treatment can lead to swift, marked resolution of symptoms. We present a patient with long-standing CD who presented with gum bleeding and was found to have scurvy.


greenmedinfo--2020-08-08--The practice of yoga may be a useful non-pharmacologic adjunctive treatment for depression in patien

The practice of yoga may be a useful non-pharmacologic adjunctive treatment for depression in patients with Parkinson's disease.

BACKGROUND : Parkinson 's disease ( PD ) is a neurodegenerative/neuropsychiatric disorder characterized by both motor and non-motor symptomology .
The reported prevalence of depression in patients with PD is difficult to ascertain due to overlapping somatic symptoms and failure to self-report symptoms .
Although antidepressants remain a first-line treatment , they can have adverse effects .
Recently , literature has demonstrated that due to its anti-inflammatory properties , yoga may be an effective nonpharmacologic therapy for depression .
METHODS : A search was conducted to identify randomized controlled trials ( RCTs ) published from January 2000 to January 2019 @ @ @ @ @ @ @ depression and motor functioning in PD .
RESULTS : Three studies met the criteria for inclusion .
In one RCT , biweekly yoga resulted in a decrease in depression score ( P = .056 ) .
In another RCT , weekly yoga resulted in a significant decrease in depression and demonstrated that its therapeutic effects are long-lasting .
Finally , in a third RCT , no significant difference was found between control and experimental groups in depression after biweekly yoga .
However , yoga was found to be protective against worsening of depression @ @ @ @ @ @ @ the practice of yoga may be a useful nonpharmacologic adjunctive treatment for depression in patients with PD .
However , more controlled RCTs are needed to validate our conclusions .

BACKGROUND: Parkinson's disease (PD) is a neurodegenerative/neuropsychiatric disorder characterized by both motor and non-motor symptomology. The reported prevalence of depression in patients with PD is difficult to ascertain due to overlapping somatic symptoms and failure to self-report symptoms. Although antidepressants remain a first-line treatment, they can have adverse effects. Recently, literature has demonstrated that due to its anti-inflammatory properties, yoga may be an effective nonpharmacologic therapy for depression.
METHODS: A search was conducted to identify randomized controlled trials (RCTs) published from January 2000 to January 2019 that assessed the effects of yoga on depression and motor functioning in PD.
RESULTS: Three studies met the criteria for inclusion. In one RCT, biweekly yoga resulted in a decrease in depression score (P = .056). In another RCT, weekly yoga resulted in a significant decrease in depression and demonstrated that its therapeutic effects are long-lasting. Finally, in a third RCT, no significant difference was found between control and experimental groups in depression after biweekly yoga. However, yoga was found to be protective against worsening of depression.
CONCLUSIONS: Our review suggests that the practice of yoga may be a useful nonpharmacologic adjunctive treatment for depression in patients with PD. However, more controlled RCTs are needed to validate our conclusions.


greenmedinfo--2020-08-08--Yoga meditation enhances proprioception and balance in individuals diagnosed with Parkinson's diseas

Yoga meditation enhances proprioception and balance in individuals diagnosed with Parkinson's disease.

This study compared the effectiveness of two proprioceptive exercise programs for persons diagnosed with Parkinson 's disease ( PD ) .
Thirty-three patients with mild to moderate PD were randomly assigned to a yoga meditation program ( YoMed ) or to an established proprioceptive training program ( PRO ) .
Both interventions included twice weekly sessions ( 45 minutes each ) , spanning a 12-week period .
Outcome measures included : joint position sense ( JPS° , JPS° , JPS° ) and joint kinesthesia ( JKand JK ) , the Tinetti Balance Assessment Tool ( TIN ) , Falls Efficacy @ @ @ @ @ @ @ Scoring System ( BESS ) , dynamic posturography ( DMA and TIME ) and the Timed Up-and-Go Test ( TUG ) .
Test administrators were blinded to group affiliation .
Significant between-group differences favoring the YoMed group were observed for TIN ( = 0.01 , = 0.77 ) and JK ( = 0.05 , = -0.72 ) .
DMA and TIME scores significantly improved for both groups , and no adverse events were reported .
These findings indicate that the YoMed program is safe and effective for patients with PD .
Researchers should @ @ @ @ @ @ @ mind-body techniques to improve movement control and body awareness in this population .

This study compared the effectiveness of two proprioceptive exercise programs for persons diagnosed with Parkinson's disease (PD). Thirty-three patients with mild to moderate PD were randomly assigned to a yoga meditation program (YoMed) or to an established proprioceptive training program (PRO). Both interventions included twice weekly sessions (45 minutes each), spanning a 12-week period. Outcome measures included: joint position sense (JPS°, JPS°, JPS°) and joint kinesthesia (JKand JK), the Tinetti Balance Assessment Tool (TIN), Falls Efficacy Scale (FES), Balance Error Scoring System (BESS), dynamic posturography (DMA and TIME) and the Timed Up-and-Go Test (TUG). Test administrators were blinded to group affiliation. Significant between-group differences favoring the YoMed group were observed for TIN ( = 0.01, = 0.77) and JK( = 0.05, = -0.72). DMA and TIME scores significantly improved for both groups, and no adverse events were reported. These findings indicate that the YoMed program is safe and effective for patients with PD. Researchers should continue to examine the clinical efficacy of mind-body techniques to improve movement control and body awareness in this population.


greenmedinfo--2020-08-08--This meta-analysis indicated that both dietary linoleic acid intake and serum linoleic acid level we

This meta-analysis indicated that both dietary linoleic acid intake and serum linoleic acid level were associated with decreased risk of breast cancer.

OBJECTIVE : Prior studies on linoleic acid , the predominant n-6 fatty acid , and breast cancer risk have generated inconsistent results .
We performed a meta-analysis to summarize the evidence regarding the relationship of dietary and serum linoleic acid with breast cancer risk .
DESIGN : Pertinent studies were identified by a search of PubMed and EMBASE .
The fixed- or random-effect pooled measure was selected based on between-study heterogeneity .
RESULTS : Eight prospective cohort studies and four prospective nested case-control studies , involving 10 410 breast cancer events from 358 955 adult females across different countries , @ @ @ @ @ @ @ with the lowest level of linoleic acid , the pooled relative risk ( RR ; 95 % CI ) of breast cancer was 0·98 ( 0·93 , 1·04 ) for the highest level of linoleic acid .
The pooled RR ( 95 % CI ) for dietary and serum linoleic acid were 0·99 ( 0·92 , 1·06 ) and 0·98 ( 0·88 , 1·08 ) , respectively .
The RR ( 95 % CI ) of breast cancer was 0·97 ( 0·91 , 1·04 ) , 0·95 ( 0·85 , 1·07 ) , @ @ @ @ @ @ @ 0·98 ( 0·87 , 1·10 ) and 0·99 ( 0·85 , 1·14 ) for linoleic acid intake of 5 , 10 , 15 , 20 and 25 g/d , respectively .
The risk of breast cancer decreased by 1 % ( RR=0·99 ; 95 % CI 0·93 , 1·05 ) for every 10 g/d increment in linoleic acid intake .
CONCLUSIONS : This meta-analysis indicated that both dietary linoleic acid intake and serum linoleic acid level were associated with decreased risk of breast cancer , although none of the associations were statistically significant @ @ @ @ @ @

OBJECTIVE: Prior studies on linoleic acid, the predominant n-6 fatty acid, and breast cancer risk have generated inconsistent results. We performed a meta-analysis to summarize the evidence regarding the relationship of dietary and serum linoleic acid with breast cancer risk.
DESIGN: Pertinent studies were identified by a search of PubMed and EMBASE. The fixed- or random-effect pooled measure was selected based on between-study heterogeneity.
RESULTS: Eight prospective cohort studies and four prospective nested case-control studies, involving 10 410 breast cancer events from 358 955 adult females across different countries, were included in present study. Compared with the lowest level of linoleic acid, the pooled relative risk (RR; 95 % CI) of breast cancer was 0·98 (0·93, 1·04) for the highest level of linoleic acid. The pooled RR (95 % CI) for dietary and serum linoleic acid were 0·99 (0·92, 1·06) and 0·98 (0·88, 1·08), respectively. The RR (95 % CI) of breast cancer was 0·97 (0·91, 1·04), 0·95 (0·85, 1·07), 0·96 (0·86, 1·07), 0·98 (0·87, 1·10) and 0·99 (0·85, 1·14) for linoleic acid intake of 5, 10, 15, 20 and 25 g/d, respectively. The risk of breast cancer decreased by 1 % (RR=0·99; 95 % CI 0·93, 1·05) for every 10 g/d increment in linoleic acid intake.
CONCLUSIONS: This meta-analysis indicated that both dietary linoleic acid intake and serum linoleic acid level were associated with decreased risk of breast cancer, although none of the associations were statistically significant. Further investigations are warranted.


greenmedinfo--2020-08-08--Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting against pree

Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting against preeclampsia.

BACKGROUND : Preeclampsia has ranked as one of the leading causes of both maternal and prenatal morbidity and mortality around the world .
The hypotensive effect of coenzyme Q10 has been widely reported in preeclampsia rat model .
However , the detailed mechanism remains unclear .
METHODS : L-NAME was utilized to establish the preeclampsia rat model .
Biomarker assessments were performed to identify the levels of vascular factors including soluble fms-like tyrosine kinase ( sFlt-1 ) and placental growth factor ( PlGF ) , the circulating cytokines including interleukin 6 , tumor necrosis factorαand interleukin 1β , and oxidative @ @ @ @ @ @ @ glutathione , superoxide dismutase , glutathione peroxidase and Catalase .
QRT-PCR was used to demonstrate the levels of cytokines in placenta tissues and Western blot was performed to estimate the nuclear factor-erythroid 2-like 2 ( Nrf2 ) and heme oxygenase 1 ( HO-1 ) protein levels .
RESULTS : Coenzyme Q10-treatment decreased the blood pressure in rat model with preeclampsia by regulating the circulating levels of sFlt-1 and PlGF .
Coenzyme Q10 attenuated serum and placental inflammation and oxidative stress in L-NAME-induced preeclampsia rats .
Coenzyme Q10 activated the placental Nrf2/HO-1 pathway in @ @ @ @ @ @ @ Q10 attenuated placental inflammatory and oxidative stress , thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway .

BACKGROUND: Preeclampsia has ranked as one of the leading causes of both maternal and prenatal morbidity and mortality around the world. The hypotensive effect of coenzyme Q10 has been widely reported in preeclampsia rat model. However, the detailed mechanism remains unclear.
METHODS: L-NAME was utilized to establish the preeclampsia rat model. Biomarker assessments were performed to identify the levels of vascular factors including soluble fms-like tyrosine kinase (sFlt-1) and placental growth factor (PlGF), the circulating cytokines including interleukin 6, tumor necrosis factorαand interleukin 1β, and oxidative stress factors including malondialdehyde, HO, glutathione, superoxide dismutase, glutathione peroxidase and Catalase. QRT-PCR was used to demonstrate the levels of cytokines in placenta tissues and Western blot was performed to estimate the nuclear factor-erythroid 2-like 2 (Nrf2) and heme oxygenase 1 (HO-1) protein levels.
RESULTS: Coenzyme Q10-treatment decreased the blood pressure in rat model with preeclampsia by regulating the circulating levels of sFlt-1 and PlGF. Coenzyme Q10 attenuated serum and placental inflammation and oxidative stress in L-NAME-induced preeclampsia rats. Coenzyme Q10 activated the placental Nrf2/HO-1 pathway in L-NAME-induced preeclampsia rats.
CONCLUSION: Coenzyme Q10 attenuated placental inflammatory and oxidative stress, thereby protecting the rats against preeclampsia by activating the Nrf2/HO-1 pathway.


greenmedinfo--2020-08-08--Serum coenzyme Q10 levels are decreased in critically-Ill septic patients.

BACKGROUND : The increased oxidative stress resulting from the inflammatory responses in sepsis initiates changes in mitochondrial function which may result in organ damage , the most common cause of death in the intensive care unit ( ICU ) .
Deficiency of coenzyme Q10 ( CoQ10 ) , a key cofactor in the mitochondrial respiratory chain , could potentially disturb mitochondrial bioenergetics and oxidative stress , and may serve as a biomarker of mitochondrial dysfunction .
Hence , we aimed to investigate in initially non-septic patients whether CoQ10 levels are decreased in sepsis and septic shock compared to ICU admission @ @ @ @ @ @ @ severity scores , inflammatory biomarkers , and ICU outcomes .
METHODS : Observational retrospective analysis on 86 mechanically-ventilated , initially non-septic , ICU patients .
CoQ10 was sequentially measured on ICU admission , sepsis , septic shock or at ICU discharge .
CoQ10 was additionally measured in 25 healthy controls .
Inflammatory biomarkers were determined at baseline and sepsis .
RESULTS : On admission , ICU patients who developed sepsis had lower CoQ10 levels compared to healthy controls ( 0.89 vs. 1.04µg/ml , < 0.05 ) , while at sepsis and septic shock @ @ @ @ @ @ @ < 0.001 and 0.42µg/ml ; < 0.0001 , respectively , from admission ) .
In ICU patients who did not develop sepsis , admission CoQ10 levels were also lower than healthy subjects ( 0.81µg/ml ; < 0.001 ) and were maintained at the same levels until discharge .
CONCLUSION : CoQ10 levels in critically-ill patients are low on ICU admission compared to healthy controls and exhibit a further decrease in sepsis and septic shock .
These results suggest that sepsis severity leads to CoQ10 depletion .

BACKGROUND: The increased oxidative stress resulting from the inflammatory responses in sepsis initiates changes in mitochondrial function which may result in organ damage, the most common cause of death in the intensive care unit (ICU). Deficiency of coenzyme Q10 (CoQ10), a key cofactor in the mitochondrial respiratory chain, could potentially disturb mitochondrial bioenergetics and oxidative stress, and may serve as a biomarker of mitochondrial dysfunction. Hence, we aimed to investigate in initially non-septic patients whether CoQ10 levels are decreased in sepsis and septic shock compared to ICU admission, and to evaluate its associations with severity scores, inflammatory biomarkers, and ICU outcomes.
METHODS: Observational retrospective analysis on 86 mechanically-ventilated, initially non-septic, ICU patients. CoQ10 was sequentially measured on ICU admission, sepsis, septic shock or at ICU discharge. CoQ10 was additionally measured in 25 healthy controls. Inflammatory biomarkers were determined at baseline and sepsis.
RESULTS: On admission, ICU patients who developed sepsis had lower CoQ10 levels compared to healthy controls (0.89 vs. 1.04µg/ml,<0.05), while at sepsis and septic shock CoQ10 levels decreased further (0.63µg/ml;<0.001 and 0.42µg/ml;<0.0001, respectively, from admission). In ICU patients who did not develop sepsis, admission CoQ10 levels were also lower than healthy subjects (0.81µg/ml;<0.001) and were maintained at the same levels until discharge.
CONCLUSION: CoQ10 levels in critically-ill patients are low on ICU admission compared to healthy controls and exhibit a further decrease in sepsis and septic shock. These results suggest that sepsis severity leads to CoQ10 depletion.


greenmedinfo--2020-08-08--Coenzyme Q10 could be beneficial in women with infertility undergoing assisted reproductive technolo

Coenzyme Q10 could be beneficial in women with infertility undergoing assisted reproductive technologies procedures.

OBJECTIVE : Increased oxidative stress has been identified as a pathogenetic mechanism in female infertility .
However , the effect of specific antioxidants , such as coenzyme Q ( CoQ ) , on the outcomes after assisted reproductive technologies ( ART ) has not been clarified .
The aim of this study was to systematically review and meta-analyze the best available evidence regarding the effect of CoQsupplementation on clinical pregnancy ( CPR ) , live birth ( LBR ) , and miscarriage rates ( MR ) compared with placebo or no-treatment in women with infertility undergoing ART .
METHODS : @ @ @ @ @ @ @ PubMed ( MEDLINE ) , Cochrane , and Scopus , from inception to March 2020 .
Data were expressed as odds ratio ( OR ) with 95 % confidence intervals ( CI ) .
The Iindex was employed for heterogeneity .
RESULTS : Five randomized-controlled trials fulfilled eligibility criteria ( 449 infertile women ; 215 in CoQgroup and 234 in placebo/no treatment group ) .
Oral supplementation of CoQresulted in an increase of CPR when compared with placebo or no-treatment ( 28.8 % vs. 14.1 % , respectively ; OR 2.44 , 95 @ @ @ @ @ @ @ ; I32 % ) .
This effect remained significant when women with poor ovarian response and polycystic ovarian syndrome were analyzed separately .
No difference between groups was observed regarding LBR ( OR 1.67 , 95 % CI 0.66-4.25 , p = 0.28 ; I34 % ) and MR ( OR 0.61 , 95 % CI 0.13-2.81 , p = 0.52 ; I0 % ) .
CONCLUSIONS : Oral supplementation of CoQmay increase CPR when compared with placebo or no-treatment , in women with infertility undergoing ART procedures , without an effect on @ @ @ @

OBJECTIVE: Increased oxidative stress has been identified as a pathogenetic mechanism in female infertility. However, the effect of specific antioxidants, such as coenzyme Q(CoQ), on the outcomes after assisted reproductive technologies (ART) has not been clarified. The aim of this study was to systematically review and meta-analyze the best available evidence regarding the effect of CoQsupplementation on clinical pregnancy (CPR), live birth (LBR), and miscarriage rates (MR) compared with placebo or no-treatment in women with infertility undergoing ART.
METHODS: A comprehensive literature search was conducted in PubMed (MEDLINE), Cochrane, and Scopus, from inception to March 2020. Data were expressed as odds ratio (OR) with 95% confidence intervals (CI). The Iindex was employed for heterogeneity.
RESULTS: Five randomized-controlled trials fulfilled eligibility criteria (449 infertile women; 215 in CoQgroup and 234 in placebo/no treatment group). Oral supplementation of CoQresulted in an increase of CPR when compared with placebo or no-treatment (28.8% vs. 14.1%, respectively; OR 2.44, 95% CI 1.30-4.59, p = 0.006; I32%). This effect remained significant when women with poor ovarian response and polycystic ovarian syndrome were analyzed separately. No difference between groups was observed regarding LBR (OR 1.67, 95% CI 0.66-4.25, p = 0.28; I34%) and MR (OR 0.61, 95% CI 0.13-2.81, p = 0.52; I0%).
CONCLUSIONS: Oral supplementation of CoQmay increase CPR when compared with placebo or no-treatment, in women with infertility undergoing ART procedures, without an effect on LBR or MR.


greenmedinfo--2020-08-08--Coenzyme Q10 - A new player in the treatment of heart failure?

Coenzyme Q10 is the only endogenously synthesized lipid with a redox function which exhibits broad tissue and intracellular distribution in @ @ @ @ @ Coenzyme Q10 supplementation were observed in several age-related diseases including heart failure .
CoQ10 ( @ @ @ @ @ significantly decreased in patients with this disease , which correlates with severity of clinical symptoms @ @ @ @ @ formulations of CoQ10 improves impaired cardiac function and clinical course of heart failure .
Current @ @ @ @ @ that CoQ10 can significantly reduce morbidity and mortality of heart failure patients in addition to @ @ @ @

Coenzyme Q10 is the only endogenously synthesized lipid with a redox function which exhibits broad tissue and intracellular distribution in mammals. Beneficial effects of Coenzyme Q10 supplementation were observed in several age-related diseases including heart failure. CoQ10 (coenzyme Q10) level is significantly decreased in patients with this disease, which correlates with severity of clinical symptoms. Supplementation with various pharmaceutical formulations of CoQ10 improves impaired cardiac function and clinical course of heart failure. Current data from clinical trials indicate that CoQ10 can significantly reduce morbidity and mortality of heart failure patients in addition to guideline recommended pharmacotherapy.


greenmedinfo--2020-08-08--Neuroprotection of coenzyme Q10 in neurodegenerative diseases.

Coenzyme Q10 ( CoQ10 ) is a component of electron transport chain and acts as an antioxidant .
It is @ @ @ @ @ against mitochondrial deficiency and oxidative stress .
Therefore , CoQ10 has received increasing attention as @ @ @ @ @ neurodegenerative diseases .
This review article focuses mainly on the structure of CoQ10 , the @ @ @ @ @ relationship between mitochondrial impairment , oxidative stress and neurodegenerative diseases .
In addition , the @ @ @ @ @ 's disease , Parkinson 's disease , and Huntington 's disease are also discussed .
@ @ @ @ @ development of successful treatment for neurodegenerative diseases are proposed .

Coenzyme Q10 (CoQ10) is a component of electron transport chain and acts as an antioxidant. It is also used for preventing neurodegeneration against mitochondrial deficiency and oxidative stress. Therefore, CoQ10 has received increasing attention as therapeutic and preventive intervention for neurodegenerative diseases. This review article focuses mainly on the structure of CoQ10, the function of CoQ10 and the relationship between mitochondrial impairment, oxidative stress and neurodegenerative diseases. In addition, the effects of CoQ10 on Alzheimer's disease, Parkinson's disease, and Huntington's disease are also discussed. Finally, future perspectives regarding development of successful treatment for neurodegenerative diseases are proposed.


greenmedinfo--2020-08-08--Coenzyme Q10 in cardiovascular and metabolic diseases.

The burden of cardiovascular and metabolic diseases is increasing with every year .
Although the management of these conditions has @ @ @ @ @ , it is still far from perfect .
With all of this in mind , @ @ @ @ @ new methods of prophylaxis and treatment .
Coenzyme Q10 ( CoQ10 ) is an essential @ @ @ @ @ .
There is growing evidence that CoQ10 is tightly linked to cardiometabolic disorders .
Its @ @ @ @ @ a variety of chronic and acute disorders .
This review analyses the role of CoQ10 @ @ @ @ @ disease , myocardial infarction , heart failure , viral myocarditis , cardiomyopathies , cardiac toxicity @ @ @ @ @ type 2 diabetes mellitus , metabolic syndrome , cardiac procedures and resuscitation .

The burden of cardiovascular and metabolic diseases is increasing with every year. Although the management of these conditions has improved greatly over the years, it is still far from perfect. With all of this in mind, there is a need for new methods of prophylaxis and treatment. Coenzyme Q10 (CoQ10) is an essential compound of the human body. There is growing evidence that CoQ10 is tightly linked to cardiometabolic disorders. Its supplementation can be useful in a variety of chronic and acute disorders. This review analyses the role of CoQ10 in hypertension, ischemic heart disease, myocardial infarction, heart failure, viral myocarditis, cardiomyopathies, cardiac toxicity, dyslipidemia, obesity, type 2 diabetes mellitus, metabolic syndrome, cardiac procedures and resuscitation.


greenmedinfo--2020-08-08--Your Body is Their Weapon - We're all Patients Now

This website is for information purposes only .
By providing the information contained herein we are not diagnosing , treating @ @ @ @ @ or preventing any type of disease or medical condition .
Before beginning any type of @ @ @ @ @ treatment regimen , it is advisable to seek the advice of a licensed healthcare professional @

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.
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greenmedinfo--2020-08-08--Dandelion extract alleviated lipopolysaccharide-induced oxidative stress.

In practical dairy production , cows are frequently subjected to inflammatory diseases , such as high-grain diet-induced subacute ruminal acidosis ( SARA ) as well as mastitis and metritis .
Under the circumstances , lipopolysaccharide ( LPS ) induces oxidative stress within the cow and in the mammary epithelial cells .
It has implications in practical production to alleviate oxidative stress and to optimize the lactational function of the mammary epithelial cells .
This study thus aimed to investigate the antioxidative effects of dandelion aqueous extract ( DAE ) on LPS-induced oxidative stress and the mechanism of DAE as an @ @ @ @ @ @ @ nuclear factor erythroid 2-related factor 2 ( Nrf2 ) pathway in the bovine mammary epithelial cell line MAC-T cells .
The cells were cultured for 48 h in six treatments including control ( without LPS and DAE ) , LPS ( 100 ng/mL ) , DAE10 ( 100 ng/mL LPS and 10μg/mL DAE ) , DAE50 ( 100 ng/mL LPS and 50 μg/mL DAE ) , DAE100 ( 100 ng/mL LPS and 100 μg/mL DAE ) , and DAE200 ( 100 ng/mL LPS and 200 μg/mL DAE ) , respectively .
The results @ @ @ @ @ @ @ LPS , and the adverse effect of LPS was suppressed with the supplementation of DAE .
Lipopolysaccharide-induced oxidative stress through enhancing reactive oxygen species ( ROS ) production , resulted in increases in oxidative damage marker concentrations , while 10 and 50 μg/mL DAE alleviated the LPS-induced oxidative stress via scavenging cellular ROS and improving antioxidant enzyme activity .
The upregulation of antioxidative gene expression in DAE treatments was promoted through activating the Nrf2 signaling pathway , with DAE at a concentration of 50 μg/mL exhibiting the highest effect .
Overall , DAE @ @ @ @ @ @ @ LPS-induced oxidative stress and asa potential inducer of the Nrf2 signaling pathway .

In practical dairy production, cows are frequently subjected to inflammatory diseases, such as high-grain diet-induced subacute ruminal acidosis (SARA) as well as mastitis and metritis. Under the circumstances, lipopolysaccharide (LPS) induces oxidative stress within the cow and in the mammary epithelial cells. It has implications in practical production to alleviate oxidative stress and to optimize the lactational function of the mammary epithelial cells. This study thus aimed to investigate the antioxidative effects of dandelion aqueous extract (DAE) on LPS-induced oxidative stress and the mechanism of DAE as an antioxidant to alleviate oxidative stress through the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in the bovine mammary epithelial cell line MAC-T cells. The cells were cultured for 48 h in six treatments including control (without LPS and DAE), LPS (100 ng/mL), DAE10 (100 ng/mL LPS and 10μg/mL DAE), DAE50 (100 ng/mL LPS and 50 μg/mL DAE), DAE100 (100 ng/mL LPS and 100 μg/mL DAE), and DAE200 (100 ng/mL LPS and 200 μg/mL DAE), respectively. The results showed that cell viability was reduced by LPS, and the adverse effect of LPS was suppressed with the supplementation of DAE. Lipopolysaccharide-induced oxidative stress through enhancing reactive oxygen species (ROS) production, resulted in increases in oxidative damage marker concentrations, while 10 and 50 μg/mL DAE alleviated the LPS-induced oxidative stress via scavenging cellular ROS and improving antioxidant enzyme activity. The upregulation of antioxidative gene expression in DAE treatments was promoted through activating the Nrf2 signaling pathway, with DAE at a concentration of 50 μg/mL exhibiting the highest effect. Overall, DAE acted as an effective antioxidant to inhibit LPS-induced oxidative stress and asa potential inducer of the Nrf2 signaling pathway.


greenmedinfo--2020-08-08--Pomegranate seed oil decreased obesity-mediated insulin resistance and the progression of hepatic fi

Pomegranate seed oil decreased obesity-mediated insulin resistance and the progression of hepatic fibrosis.

AIM : Obesity is associated with metabolic syndrome , hypertension , dyslipidemia , nonalcoholic fatty liver disease ( NAFLD ) , and type 2 diabetes .
In this study , we investigated whether the dietary supplementation of pomegranate seed oil ( PSO ) exerted a protective effect on liver lipid uptake , fibrosis , and mitochondrial function in a mouse model of obesity and insulin resistance .
METHOD : In this in vivo study , eight-week-old C57BL/6J male mice were fed with a high fat diet ( HFD ) for 24 weeks and then were divided into three groups as @ @ @ @ @ @ @ ; group ( = 6 ) ( 2 ) HF diet ; group ( = 6 ) ( 3 ) HF diet treated with PSO ( 40 mL/kg food ) ( = 6 ) for eight additional weeks starting at 24 weeks .
Physiological parameters , lipid droplet accumulation , inflammatory biomarkers , antioxidant biomarkers , mitochondrial biogenesis , insulin sensitivity , and hepatic fibrosis were determined to examine whether PSO intervention prevents obesity-associated metabolic syndrome .
RESULTS : The PSO group displayed an increase in oxygen consumption , as well as a @ @ @ @ @ @ @ ( < 0.05 ) when compared to the HFD-fed mice group .
PSO increased both the activity and expression of hepatic HO-1 , downregulated inflammatory adipokines , and decreased hepatic fibrosis .
PSO increased the levels of thermogenic genes , mitochondrial signaling , and lipid metabolism through increases in Mfn2 , OPA-1 , PRDM 16 , and PGC1α .
Furthermore , PSO upregulated obesity-mediated hepatic insulin receptor phosphorylation Tyr- , p-IRB tyr , and pAMPK , thereby decreasing insulin resistance .
CONCLUSIONS : These results indicated that PSO decreased obesity-mediated insulin resistance and @ @ @ @ @ @ @ improved liver signaling , as manifested by increased insulin receptor phosphorylation and thermogenic genes .
Furthermore , our findings indicate a potential therapeutic role for PSO in the prevention of obesity-associated NAFLD , NASH , and other metabolic disorders .

AIM: Obesity is associated with metabolic syndrome, hypertension, dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. In this study, we investigated whether the dietary supplementation of pomegranate seed oil (PSO) exerted a protective effect on liver lipid uptake, fibrosis, and mitochondrial function in a mouse model of obesity and insulin resistance.
METHOD: In this in vivo study, eight-week-old C57BL/6J male mice were fed with a high fat diet (HFD) for 24 weeks and then were divided into three groups as follows: group (1) Lean; group (= 6) (2) HF diet; group (= 6) (3) HF diet treated with PSO (40 mL/kg food) (= 6) for eight additional weeks starting at 24 weeks. Physiological parameters, lipid droplet accumulation, inflammatory biomarkers, antioxidant biomarkers, mitochondrial biogenesis, insulin sensitivity, and hepatic fibrosis were determined to examine whether PSO intervention prevents obesity-associated metabolic syndrome.
RESULTS: The PSO group displayed an increase in oxygen consumption, as well as a decrease in fasting glucose and blood pressure (<0.05) when compared to the HFD-fed mice group. PSO increased both the activity and expression of hepatic HO-1, downregulated inflammatory adipokines, and decreased hepatic fibrosis. PSO increased the levels of thermogenic genes, mitochondrial signaling, and lipid metabolism through increases in Mfn2, OPA-1, PRDM 16, and PGC1α. Furthermore, PSO upregulated obesity-mediated hepatic insulin receptor phosphorylation Tyr-, p-IRB tyr, and pAMPK, thereby decreasing insulin resistance.
CONCLUSIONS: These results indicated that PSO decreased obesity-mediated insulin resistance and the progression of hepatic fibrosis through an improved liver signaling, as manifested by increased insulin receptor phosphorylation and thermogenic genes. Furthermore, our findings indicate a potential therapeutic role for PSO in the prevention of obesity-associated NAFLD, NASH, and other metabolic disorders.


greenmedinfo--2020-08-08--Holistic Approaches: A Proven Treatment for Psychiatric Drug Withdrawal


greenmedinfo--2020-08-08--Bioactive polyphenols from pomegranate juice reduce 5-fluorouracil-induced intestinal mucositis in i

Bioactive polyphenols from pomegranate juice reduce 5-fluorouracil-induced intestinal mucositis in intestinal epithelial cells.

Intestinal epithelial cells ( IECs ) play a pivotal role in maintaining intestinal homeostasis .
Different noxious agents , among them also anticancer therapies , can impair intestinal epithelial integrity triggering inflammation and oxidative stress .
A frequent complication of chemotherapy is gastrointestinal mucositis , strongly influencing the effectiveness of therapy , increasing healthcare costs , and impairing patients ' quality of life .
Different strategies are used to treat gastrointestinal mucositis , including products from natural sources .
Our study focused on the effect of pomegranate ( L. ) juice extract on IEC-6 cells , both during inflammatory conditions @ @ @ @ @ @ @ ) .
The polyphenolic profile of pomegranate juice was characterized in detail by Online Comprehensive two dimensional Liquid Chromatography-Mass Spectrometry .
The evaluation of pomegranate juice extract in IEC-6 indicates a significant inhibition in proinflammatory factors , such as cytokines release , cyclooxygenase-2 and inducible nitric oxide synthase expression , and nitrotyrosine formation .
Pomegranate also inhibited oxidative stress and adhesion protein expression .
In 5-FU-treated IEC-6 , pomegranate also inhibited both inflammatory and oxidative stress parameters and apoptosis .
It promoted wound repair and tight junction expression .
These results suggest a @ @ @ @ @ @ @ in the treatment of intestinal inflammatory and oxidative stress states , which also occur during chemotherapy-induced mucositis .

Intestinal epithelial cells (IECs) play a pivotal role in maintaining intestinal homeostasis. Different noxious agents, among them also anticancer therapies, can impair intestinal epithelial integrity triggering inflammation and oxidative stress. A frequent complication of chemotherapy is gastrointestinal mucositis, strongly influencing the effectiveness of therapy, increasing healthcare costs, and impairing patients' quality of life. Different strategies are used to treat gastrointestinal mucositis, including products from natural sources. Our study focused on the effect of pomegranate (L.) juice extract on IEC-6 cells, both during inflammatory conditions and following treatment with 5-fluorouracil (5-FU). The polyphenolic profile of pomegranate juice was characterized in detail by Online Comprehensive two dimensional Liquid Chromatography-Mass Spectrometry. The evaluation of pomegranate juice extract in IEC-6 indicates a significant inhibition in proinflammatory factors, such as cytokines release, cyclooxygenase-2 and inducible nitric oxide synthase expression, and nitrotyrosine formation. Pomegranate also inhibited oxidative stress and adhesion protein expression. In 5-FU-treated IEC-6, pomegranate also inhibited both inflammatory and oxidative stress parameters and apoptosis. It promoted wound repair and tight junction expression. These results suggest a potential use of pomegranate as an adjuvant in the treatment of intestinal inflammatory and oxidative stress states, which also occur during chemotherapy-induced mucositis.


greenmedinfo--2020-08-08--Pomegranate fruit extract suppresses cancer progression and tumor angiogenesis of pancreatic and col

Pomegranate fruit extract suppresses cancer progression and tumor angiogenesis of pancreatic and colon cancer.

Pomegranate fruit extract contains many polyphenols and flavonoids of diverse biological importance including anticancer potential .
In cancer , the @ @ @ @ @ growth and metastasis .
Here , the antiangiogenic effect of pomegranate fruit extract against human @ @ @ @ @ and colon ( colo205 ) cell lines in the chick chorioallantoic membrane ( CAM ) @ @ @ @ @ the effect of pomegranate fruit extract on fibroblast growth factor ( FGF2 ) .
Pomegranate @ @ @ @ @ tumor weight and hemoglobin content in CAM models of pancreatic Suit-2 and colon colo205 .

Pomegranate fruit extract contains many polyphenols and flavonoids of diverse biological importance including anticancer potential. In cancer, the angiogenesis process facilitates solid cancer growth and metastasis. Here, the antiangiogenic effect of pomegranate fruit extract against human pancreatic cancer (Suit-2) and colon (colo205) cell lines in the chick chorioallantoic membrane (CAM) model was studied along with the effect of pomegranate fruit extract on fibroblast growth factor (FGF2). Pomegranate fruit extract significantly reduced the tumor weight and hemoglobin content in CAM models of pancreatic Suit-2 and colon colo205.


greenmedinfo--2020-08-08--Are the COVID Tests a Way to Surreptitiously Infect or Implant People?


greenmedinfo--2020-08-08--Pomegranate peel extract protects against carbon tetrachloride-induced nephrotoxicity.

Carbon tetrachloride ( CCl4 ) is a notorious environmental pollutant known for its toxicity .
The aim of the present study was to evaluate the possible protective effects of aqueous pomegranate peel extract ( PPE ) against CCl4 induced nephrotoxicity in mice .
Adult male mice were divided into four groups : Group one was used as the control ; Group two was treated with a daily oral dose of PPE ( 400 mg/kg ) for 15 days ; the third group was intraperitoneally injected with a dose ( 1 ml/kg ) of CCl4 twice a week for two weeks @ @ @ @ @ @ @ with the same dose of CCl4 twice a week concomitantly with a daily oral dose of PPE ( 400 mg/kg ) .
Biochemical and histopathological data were analyzed along with the gene expression levels of the antioxidant enzymes and immunohistochemistry of the kidney tissue .
CCl4 resulted in a significant increase in the serum urea and creatinine levels with detectable degenerative changes in the Bowman 's capsule and glomerulus , with cells exhibiting vacuolization and evidence of necrosis .
Co-administration of animals with CCl4 and PPE resulted in improved biochemical and histopathological conditions @ @ @ @ @ @ @ Caspase-3 and collagen fibers were reduced in mice treated with PPE .
Quantitative analysis of superoxide dismutase , catalase and glutathione peroxidase further accentuated the effects of PPE treatment significantly improving the conditions of the CCl4-administered group .
The results of the present study demonstrate that the phenolic derivative rich PPE is a potent nephroprotective agent and suppresses CCl4-induced nephrotoxicity in mice .

Carbon tetrachloride (CCl4) is a notorious environmental pollutant known for its toxicity. The aim of the present study was to evaluate the possible protective effects of aqueous pomegranate peel extract (PPE) against CCl4 induced nephrotoxicity in mice. Adult male mice were divided into four groups: Group one was used as the control; Group two was treated with a daily oral dose of PPE (400 mg/kg) for 15 days; the third group was intraperitoneally injected with a dose (1 ml/kg) of CCl4 twice a week for two weeks; and the final group was injected with the same dose of CCl4 twice a week concomitantly with a daily oral dose of PPE (400 mg/kg). Biochemical and histopathological data were analyzed along with the gene expression levels of the antioxidant enzymes and immunohistochemistry of the kidney tissue. CCl4 resulted in a significant increase in the serum urea and creatinine levels with detectable degenerative changes in the Bowman's capsule and glomerulus, with cells exhibiting vacuolization and evidence of necrosis. Co-administration of animals with CCl4 and PPE resulted in improved biochemical and histopathological conditions. Similarly, increased production of the Caspase-3 and collagen fibers were reduced in mice treated with PPE. Quantitative analysis of superoxide dismutase, catalase and glutathione peroxidase further accentuated the effects of PPE treatment significantly improving the conditions of the CCl4-administered group. The results of the present study demonstrate that the phenolic derivative rich PPE is a potent nephroprotective agent and suppresses CCl4-induced nephrotoxicity in mice.


greenmedinfo--2020-08-08--The effect of concentrated pomegranate juice consumption on risk factors of cardiovascular diseases

The effect of concentrated pomegranate juice consumption on risk factors of cardiovascular diseases in women with polycystic ovary syndrome.

Polycystic ovary syndrome ( PCOS ) is associated with insulin resistance and dyslipidemia .
Pomegranate juice is a rich source @ @ @ @ @ blood pressure , lipid profile , and other risk factors of cardiovascular diseases ( CVDs @ @ @ @ @ examined the effects of pomegranate juice consumption on the clinical outcomes of PCOS .
This @ @ @ @ @ effects of concentrated pomegranate juice ( CPJ ) consumption on risk factors of CVDs in @ @ @ @ @ this randomized clinical trial , 44 PCOS women with an age range of 18-40 years @ @ @ @ @ BMI ) of ≥25 kg/mwere recruited .
They were randomly allocated to the CPJ ( @ @ @ @ @ control ( n = 22 ) groups , and followed for 8 weeks .
Anthropometric @ @ @ @ @ and biochemical parameters were measured at baseline and at the end of the trial .
@ @ @ @ @ , CPJ consumption significantly reduced systolic ( -9.77 ± 1.46 vs. -1.18 ± 1.46 mmHg @ @

Polycystic ovary syndrome (PCOS) is associated with insulin resistance and dyslipidemia. Pomegranate juice is a rich source of polyphenols that may improve blood pressure, lipid profile, and other risk factors of cardiovascular diseases (CVDs). No study has examined the effects of pomegranate juice consumption on the clinical outcomes of PCOS. This study aimed to examine the effects of concentrated pomegranate juice (CPJ) consumption on risk factors of CVDs in women with PCOS. In this randomized clinical trial, 44 PCOS women with an age range of 18-40 years and body mass index (BMI) of ≥25 kg/mwere recruited. They were randomly allocated to the CPJ (n = 22) and control (n = 22) groups, and followed for 8 weeks. Anthropometric measures, blood pressure, and biochemical parameters were measured at baseline and at the end of the trial. Compared with the control group, CPJ consumption significantly reduced systolic (-9.77 ± 1.46 vs. -1.18 ± 1.46 mmHg, p < .001) and diastolic (-3.87 ± 1.36 vs. 0.30 ± 1.36 mmHg, p = .05) blood pressure, serum triglyceride (TG) levels (-7.82 ± 6.32 vs. 16.63 ± 6.32 mg/dl, p = .01), TG/high-density lipoprotein-cholesterol (HDL-C) ratio (-0.39 ± 0.24 vs. 0.66 ± 0.24, p = .007), and increased serum concentrations of low-density lipoprotein-cholesterol (LDL-C) (6.03 ± 2.47 vs. -1.98 ± 2.47 mg/dl, p = .04) and HDL-C (1.93 ± 1.10 vs. -1.78 ± 1.10 mg/dl, p = .03). These findings were obtained after taking baseline measurements and potential confounders into account. No adverse event or complication was reported due to CPJ consumption throughout the study. We found that CPJ consumption has a beneficial effect on blood pressure, serum concentrations of TG and HDL-C, and TG/HDL-C ratio in women with PCOS. However, this juice could increase serum LDL-C levels in these patients. This trial was registered at www.irct.ir as IRCT20191109045383N1.


greenmedinfo--2020-08-08--Consumption of Brazil nuts modulates serum creatine kinase activity in patients regularly using stat

Consumption of Brazil nuts modulates serum creatine kinase activity in patients regularly using statins.

BACKGROUND & AIMS : Although the mechanisms by which statins promote muscle disorders remain unclear , supplementation with dietary antioxidants @ @ @ @ @ effects .
This study aimed to investigate whether the consumption of Brazil nuts modulates serum @ @ @ @ @ activity in patients regularly using statins .
METHODS : The study was performed in the @ @ @ @ @ Hospital .
Thirty-two patients in regular use of statins were divided according to CK activity @ @ @ @ @ or G2 : normal ) and received one unit of Brazil nut daily for 3 @ @ @ @ @ blood selenium ( Se ) concentrations , erythrocyte glutathioneperoxidase ( GPX ) activity , oxidative @ @ @ @ @ activity were evaluated before and after supplementation .
RESULTS : In both groups , supplementation @ @ @ @ @ for 3 months contributed to achieve decreased levels of CK activity in serum , with @ @ @ @ @ erythrocyte Se concentrations ( p CONCLUSION : Brazil nut consumption enhanced the control of CK @ @ @ @ @ biomarkers in patients using statins but did not modulate mRNA expression of selenoproteins .

BACKGROUND & AIMS: Although the mechanisms by which statins promote muscle disorders remain unclear, supplementation with dietary antioxidants may mitigate statins' side effects. This study aimed to investigate whether the consumption of Brazil nuts modulates serum creatine kinase (CK) activity in patients regularly using statins.
METHODS: The study was performed in the Ribeirão Preto Medical School University Hospital. Thirty-two patients in regular use of statins were divided according to CK activity levels (G1: increased or G2: normal) and received one unit of Brazil nut daily for 3 months. Body composition, blood selenium (Se) concentrations, erythrocyte glutathioneperoxidase (GPX) activity, oxidative stress parameters, and CK activity were evaluated before and after supplementation.
RESULTS: In both groups, supplementation with one Brazil nut daily for 3 months contributed to achieve decreased levels of CK activity in serum, with positive changes in plasma and erythrocyte Se concentrations (p < 0.0001), and increased levels of GPX activity. Among the parameters related to curbing of oxidative stress, we observed reduced levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in both groups after supplementation. We also found a moderately negative association between CK and GPX activity (r = -41; p < 0.02). Expression of selenoproteins GPX1, SELENOP, and SELENON after Brazil nut supplementation was unchanged.
CONCLUSION: Brazil nut consumption enhanced the control of CK activity by improving oxidative stress biomarkers in patients using statins but did not modulate mRNA expression of selenoproteins.


greenmedinfo--2020-08-08--Studies conducted in animal models showed the ability of dietary nuts in improving biomarkers of oxi

Studies conducted in animal models showed the ability of dietary nuts in improving biomarkers of oxidative stress.

Atherosclerosis is related to fat accumulation in the arterial walls and vascular stiffening , and results in acute coronary syndrome which is commonly associated with acute myocardial infarction .
Oxidative stress participates in the pathogenesis of atherosclerosis .
Thus , the inclusion of food sources of dietary antioxidants , such as different kinds of nuts , may improve biomarkers related to oxidative stress , contributing to a possible reduction in atherosclerosis progression .
This article has briefly highlighted the interaction between oxidative stress , atherosclerosis , and cardiovascular disease , in addition to the effect of the consumption of different @ @ @ @ @ @ @ vitamin E-on biomarkers of oxidative stress in primary and secondary cardiovascular prevention .
Studiessuggest that nuts may exert antioxidant effects by DNA repair mechanisms , lipid peroxidation prevention , modulation of the signaling pathways , and inhibition of the MAPK pathways through the suppression of NF-κB and activation of the Nrf2 pathways .
Studies conducted in animal models showed the ability of dietary nuts in improving biomarkers of oxidative stress , such as oxLDL and GPx .
However , clinical trials in humans have not been conclusive , especially with regards to the @ @ @ @ @ @

Atherosclerosis is related to fat accumulation in the arterial walls and vascular stiffening, and results in acute coronary syndrome which is commonly associated with acute myocardial infarction. Oxidative stress participates in the pathogenesis of atherosclerosis. Thus, the inclusion of food sources of dietary antioxidants, such as different kinds of nuts, may improve biomarkers related to oxidative stress, contributing to a possible reduction in atherosclerosis progression. This article has briefly highlighted the interaction between oxidative stress, atherosclerosis, and cardiovascular disease, in addition to the effect of the consumption of different nuts and related dietary antioxidants-like polyphenols and vitamin E-on biomarkers of oxidative stress in primary and secondary cardiovascular prevention. Studiessuggest that nuts may exert antioxidant effects by DNA repair mechanisms, lipid peroxidation prevention, modulation of the signaling pathways, and inhibition of the MAPK pathways through the suppression of NF-κB and activation of the Nrf2 pathways. Studies conducted in animal models showed the ability of dietary nuts in improving biomarkers of oxidative stress, such as oxLDL and GPx. However, clinical trials in humans have not been conclusive, especially with regards to the secondary prevention of cardiovascular disease.


greenmedinfo--2020-08-08--Increasing total consumption of nuts and intake of individual types of nuts was associated with a su

Increasing total consumption of nuts and intake of individual types of nuts was associated with a subsequent lower risk of cardiovascular disease.

Background We aim to evaluate the association of within-individual changes in consumption of total and specific types of nuts and the subsequent risk of incident cardiovascular disease ( CVD ) in US men and women .
Methods and Results We included 34 103 men from the HPFS ( Health Professionals Follow-Up Study ) ( 1986-2012 ) , 77 815 women from the NHS ( Nurses ' Health Study ) ( 1986-2012 ) , and 80 737 women from the NHS II ( 1991-2013 ) .
We assessed nut consumption every 4 years using validated food frequency questionnaires .
We used @ @ @ @ @ @ @ examine the association between 4-year changes in nut consumption and risk of confirmed CVD end points in the subsequent 4 years .
Per 0.5 serving/day increase in total nut consumption was associated with lower risk of CVD ( relative risk [ RR ] , 0.92 ; 95 % CI , 0.86-0.98 ) , coronary heart disease ( RR , 0.94 ; 95 % CI , 0.89-0.99 ) , and stroke ( RR , 0.89 ; 95 % CI , 0.83-0.95 ) .
Compared with individuals who remained nonconsumers in a 4-year interval , @ @ @ @ @ @ @ nuts ( ≥0.5 servings/day ) had a lower risk of CVD ( RR , 0.75 ; 95 % CI , 0.67-0.84 ) , coronary heart disease ( RR , 0.80 ; 95 % CI , 0.69-0.93 ) , and stroke ( RR , 0.68 ; 95 % CI , 0.57-0.82 ) in next 4 years .
Individuals who decreased nut consumption by ≥0.50 servings/day had a higher risk of developing CVD ( RR , 1.14 ; 95 % CI , 0.99-1.32 ) , coronary heart disease ( RR , 1.06 ; 95 % @ @ @ @ @ @ @ ( RR , 1.28 ; 95 % CI , 1.02-1.60 ) when compared with those who maintained their nut consumption .
Conclusions Increasing total consumption of nuts and intake of individual types of nuts ( eg , walnuts , other tree nuts , and peanuts ) was associated with a subsequent lower risk of CVD .
These data support the role of nut intake in the primary prevention of CVD .
Registration URL : https : //www.clinicaltrials.gov .
Unique identifiers : NCT00005152 and NCT00005182 .

Background We aim to evaluate the association of within-individual changes in consumption of total and specific types of nuts and the subsequent risk of incident cardiovascular disease (CVD) in US men and women. Methods and Results We included 34 103 men from the HPFS (Health Professionals Follow-Up Study) (1986-2012), 77 815 women from the NHS (Nurses' Health Study) (1986-2012), and 80 737 women from the NHS II (1991-2013). We assessed nut consumption every 4 years using validated food frequency questionnaires. We used multivariable Cox proportional hazards regression models to examine the association between 4-year changes in nut consumption and risk of confirmed CVD end points in the subsequent 4 years. Per 0.5 serving/day increase in total nut consumption was associated with lower risk of CVD (relative risk [RR], 0.92; 95% CI, 0.86-0.98), coronary heart disease (RR, 0.94; 95% CI, 0.89-0.99), and stroke (RR, 0.89; 95% CI, 0.83-0.95). Compared with individuals who remained nonconsumers in a 4-year interval, those who had higher consumption of total nuts (≥0.5 servings/day) had a lower risk of CVD (RR, 0.75; 95% CI, 0.67-0.84), coronary heart disease (RR, 0.80; 95% CI, 0.69-0.93), and stroke (RR, 0.68; 95% CI, 0.57-0.82) in next 4 years. Individuals who decreased nut consumption by ≥0.50 servings/day had a higher risk of developing CVD (RR, 1.14; 95% CI, 0.99-1.32), coronary heart disease (RR, 1.06; 95% CI, 0.88-1.28), and stroke (RR, 1.28; 95% CI, 1.02-1.60) when compared with those who maintained their nut consumption. Conclusions Increasing total consumption of nuts and intake of individual types of nuts (eg, walnuts, other tree nuts, and peanuts) was associated with a subsequent lower risk of CVD. These data support the role of nut intake in the primary prevention of CVD. Registration URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00005152 and NCT00005182.


greenmedinfo--2020-08-09--Anticancer activity of emodin is associated with downregulation of CD155.

Emodin is a Chinese herb-derived compound that exhibits a variety of pharmacological benefits .
Although emodin has been shown to inhibit growth of cancer cells , its antineoplastic function is incompletely understood .
CD155 is a member of poliovirus receptor-related ( PRR ) family of adhesion molecules ; it is constitutively expressed on many tumor cell lines and tissues and has diverse functions .
CD155 has been reported to mediate activation of T cells via CD226 or inhibition of T cells via T-cell immunoreceptor with Ig and ITIM domains ( TIGIT ) .
In addition , CD155 may play a @ @ @ @ @ @ @ .
In this study , we tested the ability of emodin to modulate CD155 expression in cancer cells .
We found that emodin significantly decreased the expression of CD155 in tumor cells and inhibited tumor cell proliferation and migration , and induced cell-cycle arrest at G2/M phase .
The tumor inhibitory effects of emodin were lost with CD155 knockdown .
Furthermore , emodin was used to treat mice bearing B16 melanoma .
It was shown that emodin attenuated tumor growth accompanied by suppressing CD155 expression .
Therefore , we propose that emodin could @ @ @ @ @ @ @ properties of emodin are at least partially CD155 dependent .
Our study provides new insights into the mechanisms by which emodin inhibits tumor growth .

Emodin is a Chinese herb-derived compound that exhibits a variety of pharmacological benefits. Although emodin has been shown to inhibit growth of cancer cells, its antineoplastic function is incompletely understood. CD155 is a member of poliovirus receptor-related (PRR) family of adhesion molecules; it is constitutively expressed on many tumor cell lines and tissues and has diverse functions. CD155 has been reported to mediate activation of T cells via CD226 or inhibition of T cells via T-cell immunoreceptor with Ig and ITIM domains (TIGIT). In addition, CD155 may play a critical role through non-immunological mechanisms in cancer. In this study, we tested the ability of emodin to modulate CD155 expression in cancer cells. We found that emodin significantly decreased the expression of CD155 in tumor cells and inhibited tumor cell proliferation and migration, and induced cell-cycle arrest at G2/M phase. The tumor inhibitory effects of emodin were lost with CD155 knockdown. Furthermore, emodin was used to treat mice bearing B16 melanoma. It was shown that emodin attenuated tumor growth accompanied by suppressing CD155 expression. Therefore, we propose that emodin could inhibit tumor growth, and the antineoplastic properties of emodin are at least partially CD155 dependent. Our study provides new insights into the mechanisms by which emodin inhibits tumor growth.


greenmedinfo--2020-08-09--Emodin might be a promising therapeutic agent for allergic asthma.

BACKGROUND This study investigated the effects and underlying mechanisms of emodin on cough variant asthma ( CVA ) in mice .
MATERIAL AND METHODS The bronchial asthma mouse model was successfully established by use of ovalbumin ( OVA ) sensitization and challenge .
The BALB/c mice were divided into 6 groups : a control group , an OVA model without or with emodin ( 15 , 30 , 60 mg/kg ) group , and a dexamethasone ( 0.5 mg/g ) group .
The effect of the treatment was determined by measuring airway responsiveness .
The levels of immunoglobulin molecules , @ @ @ @ @ @ @ lavage fluid ( BALF ) and serum , were determined by ELISA .
The lung tissues were stained by hematoxylin-eosin ( HE ) .
The expressions of Notch receptors ( Notch 1-3 ) and Delta-like ( DLL ) 4 in the lung tissues were detected by RT-PCR and Western blot analysis .
RESULTS Compared with the model group , emodin treatment significantly increased the levels of immunoglobulin E ( IgE ) and IgG1/IgG2a in BALF and serum ( p < 0.05 ) .
HE results indicated that emodin inhibited the infiltration of inflammatory @ @ @ @ @ @ @ of inflammatory cytokines , interleukin ( IL ) -5 , IL-17 , and interferon ( IFN ) -γ in BALF and serum ( p < 0.05 ) .
Furthermore , the expressions of Notch 1 , 2 , 3 , and DLL4 in lung tissue were inhibited by emodin treatment .
CONCLUSIONS The results demonstrated that emodin alleviated inflammation in CVA mice , which might be associated with suppression of the Notch pathway .
Emodin might be a promising therapeutic agent for allergic asthma .

BACKGROUND This study investigated the effects and underlying mechanisms of emodin on cough variant asthma (CVA) in mice. MATERIAL AND METHODS The bronchial asthma mouse model was successfully established by use of ovalbumin (OVA) sensitization and challenge. The BALB/c mice were divided into 6 groups: a control group, an OVA model without or with emodin (15, 30, 60 mg/kg) group, and a dexamethasone (0.5 mg/g) group. The effect of the treatment was determined by measuring airway responsiveness. The levels of immunoglobulin molecules, as well as inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum, were determined by ELISA. The lung tissues were stained by hematoxylin-eosin (HE). The expressions of Notch receptors (Notch 1-3) and Delta-like (DLL) 4 in the lung tissues were detected by RT-PCR and Western blot analysis. RESULTS Compared with the model group, emodin treatment significantly increased the levels of immunoglobulin E (IgE) and IgG1/IgG2a in BALF and serum (p<0.05). HE results indicated that emodin inhibited the infiltration of inflammatory cells and that emodin reduced the levels of inflammatory cytokines, interleukin (IL)-5, IL-17, and interferon (IFN)-γ in BALF and serum (p<0.05). Furthermore, the expressions of Notch 1, 2, 3, and DLL4 in lung tissue were inhibited by emodin treatment. CONCLUSIONS The results demonstrated that emodin alleviated inflammation in CVA mice, which might be associated with suppression of the Notch pathway. Emodin might be a promising therapeutic agent for allergic asthma.


greenmedinfo--2020-08-09--Daily consumption of vinegar can reduce the rise in blood sugar and lipid profile induced by hyperca

Daily consumption of vinegar can reduce the rise in blood sugar and lipid profile induced by hypercaloric diet.

The main objective of this study is to determine the effects of apple vinegar on the metabolic changes caused by hypercaloric diet in Wistar rats .
Apple vinegar was first analyzed to find out the total acidity , the polyphenolic and flavonoid contents , the total antioxidant capacity , and the free radical scavenging activity.study on adult male and female Wistar rats was conducted by administering a drink containing either 10 % D-glucose or water ( control ) for five weeks .
Apple vinegar is administered daily by gavage ( 2 mL/kg ) to rats fed D-glucose for 5 weeks @ @ @ @ @ @ @ content in apple vinegar was 148.02 ± 10.16 mg GAE/100 mL , flavonoid content was 22.93 ± 0.73 QE/100 mL , and total antioxidant capacity was 13.4 ± 0.47 mg AAE/100 mL .
Free radical ICapple vinegar scavenging activity ( DPPH ) was 0.74± 0.154 L/mL .
The total acidity was ( 3.24± 0.02 mg AAE/100 mL ) .
The treatment during five weeks with D-glucose leads to increased plasma glucose , lipid profile , hepatic enzyme levels , urea , and creatinine .
Simultaneous treatment with apple vinegar improves the parameters studied @ @ @ @ @ @ @ daily consumption of vinegar can reduce the rise in blood sugar and lipid profile induced by hypercaloric diet in rats .
Therefore , the use of apple vinegar would have a very beneficial effect in the prevention of metabolic disorders caused by high-caloric food .

The main objective of this study is to determine the effects of apple vinegar on the metabolic changes caused by hypercaloric diet in Wistar rats. Apple vinegar was first analyzed to find out the total acidity, the polyphenolic and flavonoid contents, the total antioxidant capacity, and the free radical scavenging activity.study on adult male and female Wistar rats was conducted by administering a drink containing either 10% D-glucose or water (control) for five weeks. Apple vinegar is administered daily by gavage (2 mL/kg) to rats fed D-glucose for 5 weeks. The results showed that the polyphenolic content in apple vinegar was 148.02 ± 10.16 mg GAE/100 mL, flavonoid content was 22.93 ± 0.73 QE/100 mL, and total antioxidant capacity was 13.4 ± 0.47 mg AAE/100 mL. Free radical ICapple vinegar scavenging activity (DPPH) was 0.74± 0.154 L/mL. The total acidity was (3.24± 0.02 mg AAE/100 mL). The treatment during five weeks with D-glucose leads to increased plasma glucose, lipid profile, hepatic enzyme levels, urea, and creatinine. Simultaneous treatment with apple vinegar improves the parameters studied. These results clearly show that the daily consumption of vinegar can reduce the rise in blood sugar and lipid profile induced by hypercaloric diet in rats. Therefore, the use of apple vinegar would have a very beneficial effect in the prevention of metabolic disorders caused by high-caloric food.


greenmedinfo--2020-08-09--Polyphenols enhance the activity of alkylating agents in leukaemia cell lines.

Polyphenols have been shown to sensitize solid tumours to alkylating agents such as cisplatin , and induce apoptosis and/or cell-cycle arrest .
Here , we assess the effects of five polyphenols alone and in combination with three alkylating agents : cisplatin , cyclophosphamide and chlorambucil in lymphoid and myeloid leukaemia cells lines , and non-tumour control cells .
In lymphoid leukaemia cell lines there was a synergistic reduction in ATP and glutathione levels , an induction of cell cycle arrest , DNA damage and apoptosis when quercetin , apigenin , emodin and rhein were combined with cisplatin and cyclophosphamide ; @ @ @ @ @ @ @ with chlorambucil .
In myeloid leukaemia cells quercetin , apigenin and emodin showed a similar synergistic effect with all alkylating agents ; however antagonistic effects were observed with some or all alkylating agents when combined with emodin , rhein and cis-stilbene .
All synergistic effects were associated with reduced glutathione levels , DNA damage and apoptosis ; whilst during antagonism the reverse effects were observed .
The combination of alkylating agents , particularly cisplatin with polyphenols could be promising for the treatment of lymphoid leukaemias , with apigenin showing the greatest effects .
@ @ @ @ @ @ @ the action of all alkylating agents , suggesting that apigenin may also be beneficial in myeloid leukaemias .

Polyphenols have been shown to sensitize solid tumours to alkylating agents such as cisplatin, and induce apoptosis and/or cell-cycle arrest. Here, we assess the effects of five polyphenols alone and in combination with three alkylating agents: cisplatin, cyclophosphamide and chlorambucil in lymphoid and myeloid leukaemia cells lines, and non-tumour control cells. In lymphoid leukaemia cell lines there was a synergistic reduction in ATP and glutathione levels, an induction of cell cycle arrest, DNA damage and apoptosis when quercetin, apigenin, emodin and rhein were combined with cisplatin and cyclophosphamide; and when apigenin and rhein were combined with chlorambucil. In myeloid leukaemia cells quercetin, apigenin and emodin showed a similar synergistic effect with all alkylating agents; however antagonistic effects were observed with some or all alkylating agents when combined with emodin, rhein and cis-stilbene. All synergistic effects were associated with reduced glutathione levels, DNA damage and apoptosis; whilst during antagonism the reverse effects were observed. The combination of alkylating agents, particularly cisplatin with polyphenols could be promising for the treatment of lymphoid leukaemias, with apigenin showing the greatest effects. Likewise in myeloid cells apigenin also synergised the action of all alkylating agents, suggesting that apigenin may also be beneficial in myeloid leukaemias.


greenmedinfo--2020-08-09--Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts.

Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis .
Emodin has been used as a natural medicine against several @ @ @ @ @ of this study is to determine the effects of emodin on cardiac fibrosis and the @ @ @ @ @ administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological @ @ @ @ @ induced by transaortic constriction ( TAC ) and suppressed activation of cardiac fibroblasts induced by @ @ @ @ @ .
Emodin upregulated expression of metastasis associated protein 3 ( MTA3 ) and restored the @ @ @ @ @ of cardiac fibrosis .
Moreover , overexpression of MTA3 promoted cardiac fibrosis ; in contrast @ @ @ @ @ the inhibitory effect of emodin on fibroblast activation .
Our findings unraveled the potential of @ @ @ @ @ MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis .

Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. Emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction (TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II (AngII). Emodin upregulated expression of metastasis associated protein 3 (MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis; in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosisupregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.


greenmedinfo--2020-08-09--The anti-hepatitis B virus therapeutic potential of anthraquinones derived from Aloe vera.

Although the approved hepatitis B virus ( HBV ) -polymerase inhibitors ( e.g.
, lamivudine ) often lead to drug-resistance , several natural products have shown promising efficacies .
Though Aloe vera ( AV ) gel and its constituents are shown inhibitors of many viruses , their anti-HBV activity still remains elusive .
We therefore , tested the anti-HBV potential of AV extract and its anthraquinones in hepatoma cells , including molecular docking , high-performance thin layer chromatography ( HPTLC ) , and cytochrome P450 ( CYP3A4 ) activation analyses .
Our anti-HBV assays ( HBsAg/HBeAg Elisa ) showed maximal @ @ @ @ @ @ @ ( ~83 % ) > chrysophanol ( ~62 % ) > aloin B ( ~61 % ) > AV extract ( ~37 % ) in HepG2.2.15 cells .
Interestingly , the effect of aloe-emodin was comparable with lamivudine ( ~86 % ) .
Moreover , sequential treatment with lamivudine ( pulse ) followed by aloe-emodin ( chase ) enhanced the efficacy of monotherapy by ~12 % .
Docking ( AutoDock Vina ) of the anthraquinones indicated strong interactions with HBV-polymerase residues that formed stable complexes with high Gibbs 's free energy .
Further @ @ @ @ @ @ @ by validated HPTLC in AV extract strongly endorsed its anti-HBV potential .
In addition , our luciferase-reporter gene assay of transfected HepG2 cells showed moderate induction of CYP3A4 by aloe-emodin .
In conclusion , this is the first report on anti-HBV potential of AV-derived anthraquinones , possibly via HBV-polymerase inhibition .
Of these , although aloin B exhibits novel antiviral effect , aloe-emodin appears as the most promising anti-HBV natural drug with CYP3A4 activating property towards its enhanced therapeutic efficacy .

Although the approved hepatitis B virus (HBV)-polymerase inhibitors (e.g., lamivudine) often lead to drug-resistance, several natural products have shown promising efficacies. Though Aloe vera (AV) gel and its constituents are shown inhibitors of many viruses, their anti-HBV activity still remains elusive. We therefore, tested the anti-HBV potential of AV extract and its anthraquinones in hepatoma cells, including molecular docking, high-performance thin layer chromatography (HPTLC), and cytochrome P450 (CYP3A4) activation analyses. Our anti-HBV assays (HBsAg/HBeAg Elisa) showed maximal inhibition of viral antigens production by aloe-emodin (~83%)>chrysophanol (~62%)>aloin B (~61%)>AV extract (~37%) in HepG2.2.15 cells. Interestingly, the effect of aloe-emodin was comparable with lamivudine (~86%). Moreover, sequential treatment with lamivudine (pulse) followed by aloe-emodin (chase) enhanced the efficacy of monotherapy by ~12%. Docking (AutoDock Vina) of the anthraquinones indicated strong interactions with HBV-polymerase residues that formed stable complexes with high Gibbs's free energy. Further, identification of aloe-emodin and aloin B by validated HPTLC in AV extract strongly endorsed its anti-HBV potential. In addition, our luciferase-reporter gene assay of transfected HepG2 cells showed moderate induction of CYP3A4 by aloe-emodin. In conclusion, this is the first report on anti-HBV potential of AV-derived anthraquinones, possibly via HBV-polymerase inhibition. Of these, although aloin B exhibits novel antiviral effect, aloe-emodin appears as the most promising anti-HBV natural drug with CYP3A4 activating property towards its enhanced therapeutic efficacy.


greenmedinfo--2020-08-09--Emodin: Its role in prostate cancer‑associated inflammation.

Prostate cancer is one of the most common malignancies diagnosed in males .
Cancer‑related inflammatory factors include tumor necrosis factor @ @ @ @ @ chemokines , transcription factors , infiltrating or circulating immune cells , reactive oxygen species , @ @ @ @ @ These are mainly associated with the local immune response at the tumor site .
Emodin @ @ @ @ @ can be isolated from the plant rhubarb among others , has been shown to exhibit @ @ @ @ @ prostate cancer .
This review summarizes the effects of emodin on prostate cancer and analyzes @ @ @ @ @ cancer through anti‑inflammatory pathways .
New information regarding the development of emodin derivatives including their @ @ @ @ @ effects through chemical structure modifications is also reviewed .

Prostate cancer is one of the most common malignancies diagnosed in males. Cancer‑related inflammatory factors include tumor necrosis factor, inflammasomes, cytokines, chemokines, transcription factors, infiltrating or circulating immune cells, reactive oxygen species, and sex hormone receptors. These are mainly associated with the local immune response at the tumor site. Emodin, a chemical compound that can be isolated from the plant rhubarb among others, has been shown to exhibit anti‑inflammatory and anticancer properties in prostate cancer. This review summarizes the effects of emodin on prostate cancer and analyzes whether it interferes with prostate cancer through anti‑inflammatory pathways. New information regarding the development of emodin derivatives including their increased solubility and reduced side effects through chemical structure modifications is also reviewed.


greenmedinfo--2020-08-09--Emodin promotes fibroblast apoptosis and prevents epidural fibrosis through PERK pathway in rats.

BACKGROUND : Laminectomy is usually classed as a common orthopedic surgery , but postoperative epidural fibrosis often leads to less-than-desirable clinical outcomes .
As demonstrated by prior studies , emodin ( EMO ) exerts an anti-fibrotic effect .
Here , we carried out investigation into the inhibitory effect created by EMO application on epidural fibrosis after laminectomy in rats .
METHODS : The paper conducts a series of experiment .
In vitro , we observed the effect of EMO on fibroblasts by Cell Counting Kit-8 ( CCK-8 ) assay .
Apoptosis of fibroblasts induced by EMO was detected by western @ @ @ @ @ @ @ cytometry .
The results revealed that EMO was capable of inducing fibroblast apoptosis , and the proteins of PERK pathway also changed accordingly .
In vivo , the effect of EMO on epidural fibrosis in 12 male Sprague-Dawley rats was observed by histological staining .
RESULTS : CCK-8 assay indicated that EMO was effective in reducing fibroblast viability in a time- and a dose-dependent manner .
TUNEL assay and flow cytometry analysis have demonstrated that the apoptotic rate of fibroblasts increased as the EMO concentration rose .
Western blot analysis proved that EMO @ @ @ @ @ @ @ p-eIF2α and that the expression of its downstream proteins CHOP and GRP78 was also enhanced .
The expression of apoptotic protein Bax and cleaved PARP was upregulated , whereas the expression of anti-apoptotic protein Bcl-2 was downregulated .
In addition , histological and immunohistochemical analysis demonstrated that EMO functioned to inhibit epidural fibrosis and increase GRP78 expression in fibrous tissue by promoting apoptosis of fibroblasts .
CONCLUSIONS : EMO could have inhibitory effect on epidural fibrosis in a concentration-dependent manner .
The potential mechanism might be through PERK signaling pathway to promote fibroblast @ @ @ @ @ @ @ be taken as a novel method for the treatment of epidural fibrosis .

BACKGROUND: Laminectomy is usually classed as a common orthopedic surgery, but postoperative epidural fibrosis often leads to less-than-desirable clinical outcomes. As demonstrated by prior studies, emodin (EMO) exerts an anti-fibrotic effect. Here, we carried out investigation into the inhibitory effect created by EMO application on epidural fibrosis after laminectomy in rats.
METHODS: The paper conducts a series of experiment. In vitro, we observed the effect of EMO on fibroblasts by Cell Counting Kit-8 (CCK-8) assay. Apoptosis of fibroblasts induced by EMO was detected by western blot, TUNEL assay, and flow cytometry. The results revealed that EMO was capable of inducing fibroblast apoptosis, and the proteins of PERK pathway also changed accordingly. In vivo, the effect of EMO on epidural fibrosis in 12 male Sprague-Dawley rats was observed by histological staining.
RESULTS: CCK-8 assay indicated that EMO was effective in reducing fibroblast viability in a time- and a dose-dependent manner. TUNEL assay and flow cytometry analysis have demonstrated that the apoptotic rate of fibroblasts increased as the EMO concentration rose. Western blot analysis proved that EMO promoted the relative expression of p-perk and p-eIF2α and that the expression of its downstream proteins CHOP and GRP78 was also enhanced. The expression of apoptotic protein Bax and cleaved PARP was upregulated, whereas the expression of anti-apoptotic protein Bcl-2 was downregulated. In addition, histological and immunohistochemical analysis demonstrated that EMO functioned to inhibit epidural fibrosis and increase GRP78 expression in fibrous tissue by promoting apoptosis of fibroblasts.
CONCLUSIONS: EMO could have inhibitory effect on epidural fibrosis in a concentration-dependent manner. The potential mechanism might be through PERK signaling pathway to promote fibroblast apoptosis. It has a possibility to be taken as a novel method for the treatment of epidural fibrosis.


greenmedinfo--2020-08-09--Emodin and AZT synergistically inhibit the proliferation and induce apoptosis of leukemia K562 cells

Emodin and AZT synergistically inhibit the proliferation and induce apoptosis of leukemia K562 cells.

The aim of the present study was to investigate the synergistic antitumor effects of emodin and 3'‑azido‑3'‑deoxythymidine ( AZT ) on human chronic myeloid leukemia cells and to explore the possible underlying mechanisms .
The K562 cells were treated with emodin and AZT , and the rates of cell inhibition and apoptosis were determined by MTT assay and flow cytometry , respectively .
The mRNA expression of EGR1 was detected by reverse transcription‑polymerase chain reaction ( RT‑PCR ) analysis .
The expression of EGR1 was silenced using siRNA , and then protein expression of β‑catenin was detected by western blotting @ @ @ @ @ @ @ the inhibitory effect of emodin in K562 cells .
The IC50 of the emodin/AZT combination at 24 , 48 or 72 h was 23.6/235.6 , 10.2/101.6 or 5.9/58.5 µmol/l , respectively , which was significantly lower compared with the IC50 of emodin ( all > 32 µmol/l ) or AZT ( all > 320 µmol/l ) alone .
There was a dose‑dependent response to the combined emodin and AZT treatment , and the calculation of the combination index yielded values < 1 , demonstrating the synergistic effect of the combined treatment compared with @ @ @ @ @ @ @ .
Furthermore , the combination of emodin and AZT increased apoptosis in K562 cells ( P < 0.05 ) .
Apoptosis was higher in the combination group compared with that of either treatment alone or control groups .
The expression of early growth response‑1 ( EGR1 ) in K562 cells was upregulated in a time‑dependent manner .
The expression of EGR1 was higher in the combination group compared with that in the emodin or AZT alone groups .
The expression of the Wnt/β‑catenin signaling pathway in the combination group was lower compared with @ @ @ @ @ @ @ groups .
The expression of the Wnt/β‑catenin signaling pathway was significantly increased following EGR1 siRNA transfection .
These data suggest that treating K562 cells with a combination of emodin and AZT exhibits reduced toxicity and improves therapeutic efficacy , and that the growth , inhibition , apoptosis and regulation of the Wnt/β‑catenin signaling pathway in human chronic myeloid leukemia cells by emodin and AZT may be associated with the expression of EGR1 .

The aim of the present study was to investigate the synergistic antitumor effects of emodin and 3'‑azido‑3'‑deoxythymidine (AZT) on human chronic myeloid leukemia cells and to explore the possible underlying mechanisms. The K562 cells were treated with emodin and AZT, and the rates of cell inhibition and apoptosis were determined by MTT assay and flow cytometry, respectively. The mRNA expression of EGR1 was detected by reverse transcription‑polymerase chain reaction (RT‑PCR) analysis. The expression of EGR1 was silenced using siRNA, and then protein expression of β‑catenin was detected by western blotting. The results demonstrated that AZT enhanced the inhibitory effect of emodin in K562 cells. The IC50 of the emodin/AZT combination at 24, 48 or 72 h was 23.6/235.6, 10.2/101.6 or 5.9/58.5 µmol/l, respectively, which was significantly lower compared with the IC50 of emodin (all>32 µmol/l) or AZT (all>320 µmol/l) alone. There was a dose‑dependent response to the combined emodin and AZT treatment, and the calculation of the combination index yielded values<1, demonstrating the synergistic effect of the combined treatment compared with the control (P<0.05). Furthermore, the combination of emodin and AZT increased apoptosis in K562 cells (P<0.05). Apoptosis was higher in the combination group compared with that of either treatment alone or control groups. The expression of early growth response‑1 (EGR1) in K562 cells was upregulated in a time‑dependent manner. The expression of EGR1 was higher in the combination group compared with that in the emodin or AZT alone groups. The expression of the Wnt/β‑catenin signaling pathway in the combination group was lower compared with that in the emodin or AZT alone groups. The expression of the Wnt/β‑catenin signaling pathway was significantly increased following EGR1 siRNA transfection. These data suggest that treating K562 cells with a combination of emodin and AZT exhibits reduced toxicity and improves therapeutic efficacy, and that the growth, inhibition, apoptosis and regulation of the Wnt/β‑catenin signaling pathway in human chronic myeloid leukemia cells by emodin and AZT may be associated with the expression of EGR1.


greenmedinfo--2020-08-09--Aloe emodin reduces cardiac inflammation induced by a high-fat diet.

Background : Aloe emodin ( AE ) is a lipid-lowering agent , which could be used to treat hyperlipidemia , thereby reducing the risk of cardiovascular disease .
Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages .
Purpose : The purpose of this study is to evaluate the potential roles and mechanisms of AE in hyperlipidemia-induced oxidative stress and inflammation in the heart.. We established a hyperlipidemia-induced cardiac inflammation model in rats and cells then administered AE and observed its effect on hyperlipidemia-induced cardiac inflammation .
Methods : We used a @ @ @ @ @ @ @ high-fat diet ( HFD ) for 10 weeks and cell culture experimental models of inflammation in the heart stimulated by PA for 14 h. Inflammatory markers were detected by qRT-PCR , WB , and immunofluorescence .
Results : We demonstrated that the expression levels of proinflammatory cytokines IL-1 , IL-6 , and TNF-were increased in the HFD group compared to the normal diet ( ND ) group , whereas AE treatment significantly reduced their levels in the myocardium .
In addition , vascular cell adhesion molecule 1 ( VCAM1 ) and intercellular adhesion @ @ @ @ @ @ @ were also inhibited by AE .
Ourstudy showed AE treatment dose-dependently decreased the expression of IL-1 , IL-6 , and TNF-were increased in the HFD group compared to the normal diet ( ND ) group , whereas AE treatment significantly reduced their levels in the myocardium .
In addition , vascular cell adhesion molecule 1 ( VCAM1 ) and intercellular adhesion molecule 1 ( ICAM-1 ) protein expressions were also inhibited by AE .
OurB , and p-P65landstudy showed AE treatment dose-dependently decreased the expression of IL-1 .
Conclusion : Taken together , @ @ @ @ @ @ @ HFD/PA-induced cardiac inflammation via inhibition of the TLR4/NF-B signaling pathway .
Thus , AE may be a promising therapeutic strategy for preventing hyperlipidemia-induced myocardial injury.B , and p-P65l .

Background: Aloe emodin (AE) is a lipid-lowering agent, which could be used to treat hyperlipidemia, thereby reducing the risk of cardiovascular disease. Recent evidence suggests that hyperlipidemia is associated with many cardiac pathological alterations and might worsen myocardial damages.
Purpose: The purpose of this study is to evaluate the potential roles and mechanisms of AE in hyperlipidemia-induced oxidative stress and inflammation in the heart.. We established a hyperlipidemia-induced cardiac inflammation model in rats and cells then administered AE and observed its effect on hyperlipidemia-induced cardiac inflammation.
Methods: We used a mouse model of hyperlipidemia caused by a high-fat diet (HFD) for 10 weeks and cell culture experimental models of inflammation in the heart stimulated by PA for 14 h. Inflammatory markers were detected by qRT-PCR, WB, and immunofluorescence.
Results: We demonstrated that the expression levels of proinflammatory cytokines IL-1, IL-6, and TNF-were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. Ourstudy showed AE treatment dose-dependently decreased the expression of IL-1, IL-6, and TNF-were increased in the HFD group compared to the normal diet (ND) group, whereas AE treatment significantly reduced their levels in the myocardium. In addition, vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM-1) protein expressions were also inhibited by AE. OurB, and p-P65landstudy showed AE treatment dose-dependently decreased the expression of IL-1.
Conclusion: Taken together, our findings disclose that AE could alleviate HFD/PA-induced cardiac inflammation via inhibition of the TLR4/NF-B signaling pathway. Thus, AE may be a promising therapeutic strategy for preventing hyperlipidemia-induced myocardial injury.B, and p-P65l.


greenmedinfo--2020-08-09--These findings suggest the potential application of MeshimaMax for cancer prevention and as suppleme

These findings suggest the potential application of MeshimaMax for cancer prevention and as supplement regimen for anticancer chemotherapy.

Natural products have attracted great interest for some time as alternative methods against cancers by fulfilling immunomodulating properties .
In this study , we investigated the activity of hot water extracts ( 120°C , > 30 min ) offresh leaves of Kumaizasa bamboo and Chaga mushroom which we called MeshimaMax , for cancer prevention and treatment by using different solid tumor models .
In the implanted mouse sarcoma S180 tumor , MeshimaMax treatment significantly inhibited tumor growth when it was applied at the early stage of tumor inoculation .
The effect was further confirmed by using carcinogen induced tumors , @ @ @ @ @ @ @ sulfate sodium ( DSS ) induced mouse colon cancer and 7,12-dimethylbenz anthracene ( DMBA ) induced rat breast cancer .
In both cases the occurrences of tumors were remarkably suppressed by administration of MeshimaMax which consists of three components above .
More importantly , when MeshimaMax was combined with an anticancer chemotherapeutic drug , the therapeutic effect was remarkably improved .
In vitro studies showed that when MeshimaMax was applied to mouse macrophage RAW264.7 cells the phagocytosis of macrophages was significantly activated , which was evaluated by using living yeast cells as well @ @ @ @ @ @ @ showed the 50 % inhibitory concentration ( IC ) was higher than 1 mg/mL and normal cells were 2-3 times more tolerant to MeshimaMax than cancer cells .
These findings suggest the potential application of MeshimaMax for cancer prevention and as supplement regimen for anticancer chemotherapy , probably functioning through activation of innate immunity , which may benefit cancer patients as an alternative supplement .

Natural products have attracted great interest for some time as alternative methods against cancers by fulfilling immunomodulating properties. In this study, we investigated the activity of hot water extracts (120°C,>30 min) offresh leaves of Kumaizasa bamboo and Chaga mushroom which we called MeshimaMax, for cancer prevention and treatment by using different solid tumor models. In the implanted mouse sarcoma S180 tumor, MeshimaMax treatment significantly inhibited tumor growth when it was applied at the early stage of tumor inoculation. The effect was further confirmed by using carcinogen induced tumors, i.e., azoxymethane (AOM)/dextran sulfate sodium (DSS) induced mouse colon cancer and 7,12-dimethylbenz anthracene (DMBA) induced rat breast cancer. In both cases the occurrences of tumors were remarkably suppressed by administration of MeshimaMax which consists of three components above. More importantly, when MeshimaMax was combined with an anticancer chemotherapeutic drug, the therapeutic effect was remarkably improved. In vitro studies showed that when MeshimaMax was applied to mouse macrophage RAW264.7 cells the phagocytosis of macrophages was significantly activated, which was evaluated by using living yeast cells as well as synthetic nanoparticles. A cytotoxicity assay showed the 50% inhibitory concentration (IC) was higher than 1 mg/mL and normal cells were 2-3 times more tolerant to MeshimaMax than cancer cells. These findings suggest the potential application of MeshimaMax for cancer prevention and as supplement regimen for anticancer chemotherapy, probably functioning through activation of innate immunity, which may benefit cancer patients as an alternative supplement.