greenmedinfo--2020-03-30--Galangin inhibits the cell progression and induces cell apoptosis through activating PTEN and Caspas

Galangin inhibits the cell progression and induces cell apoptosis through activating PTEN and Caspase-3 pathways in retinoblastoma.

Retinoblastoma is reported as a rare cancer that occurs during childhood .
Although several treatments are available for retinoblastoma , there is a need for alternative new treatment modalities for retinoblastoma with better safety and efficacy profile .
Galangin ( 3,5,7-trihydroxyflavone ) , is a flavonoid compound , which is found in high concentration in lesser galangal .
Galangin has been reported to have various bioactivities , including anti-inflammation , anti-oxidative stress and anti-cancer through various pathways .
The objective of our study was to explore the effects of galangin on the suppression of retinoblastoma in vitro and in vivo @ @ @ @ @ @ @ analysis , colony-forming analysis , wound healing analysis , immunofluorescent assay of KI-67 , we found that galangin exhibited a suppressive effect on human retinoblastoma cell proliferation and migration .
Moreover , PTEN , a tumor-suppressor , was increased by galangin in cancer cells and in tumor tissues isolated from retinoblastoma xenograft models .
Additionally , galangin reduced protein kinase B ( Akt ) phosphorylation , which was associated with PTEN up-regulation .
Galangin-reduced Akt activation and cell proliferation was abolished by PTEN knockdown , which might be associated with the over-expression of @ @ @ @ @ @ @ PIP2 ) .
Furthermore , flow cytometry , Hoechst 33258 staining and western blot assays indicated that galangin could induce apoptosis through promoting Caspase-3 pathway , which was , at least partly , dependent on PTEN expression .
Our data illustrated that galangin treatment suppressed the growth of retinoblastoma tumor in vivo by anti-proliferative and apoptogenic mechanisms .
Thus , galangin might be a safe and promising non-chemotherapeutic drug , which could be useful as an adjuvant against retinoblastoma .

Retinoblastoma is reported as a rare cancer that occurs during childhood. Although several treatments are available for retinoblastoma, there is a need for alternative new treatment modalities for retinoblastoma with better safety and efficacy profile. Galangin (3,5,7-trihydroxyflavone), is a flavonoid compound, which is found in high concentration in lesser galangal. Galangin has been reported to have various bioactivities, including anti-inflammation, anti-oxidative stress and anti-cancer through various pathways. The objective of our study was to explore the effects of galangin on the suppression of retinoblastoma in vitro and in vivo. Using MTT analysis, transwell-chamber migration analysis, colony-forming analysis, wound healing analysis, immunofluorescent assay of KI-67, we found that galangin exhibited a suppressive effect on human retinoblastoma cell proliferation and migration. Moreover, PTEN, a tumor-suppressor, was increased by galangin in cancer cells and in tumor tissues isolated from retinoblastoma xenograft models. Additionally, galangin reduced protein kinase B (Akt) phosphorylation, which was associated with PTEN up-regulation. Galangin-reduced Akt activation and cell proliferation was abolished by PTEN knockdown, which might be associated with the over-expression of phosphatidylinositol-3,4,5-triphosphate (PIP3)/diphosphate product (PIP2). Furthermore, flow cytometry, Hoechst 33258 staining and western blot assays indicated that galangin could induce apoptosis through promoting Caspase-3 pathway, which was, at least partly, dependent on PTEN expression. Our data illustrated that galangin treatment suppressed the growth of retinoblastoma tumor in vivo by anti-proliferative and apoptogenic mechanisms. Thus, galangin might be a safe and promising non-chemotherapeutic drug, which could be useful as an adjuvant against retinoblastoma.


greenmedinfo--2020-03-30--Galangin has a role in protecting dopaminergic neurons by inhibiting microglial activation.

Parkinson 's disease ( PD ) is caused by the loss of dopaminergic ( DA ) neurons in the midbrain substantia nigra ( SN ) .
Neuroinflammation , which is marked by microglial activation , plays a very important role in the pathogenesis of PD .
Pro-inflammatory mediators produced by activated microglia could damage DA neurons .
Hence , the inhibition of microglial activation may provide a new approach for treating PD .
Galangin has been shown to inhibit inflammation in a variety of diseases , but not PD .
In this study , we aimed to investigate the anti-inflammatory @ @ @ @ @ @ @ in Lipopolysaccharide ( LPS ) induced PD models .
We first examined the protective effect of galangin in the LPS-induced PD rat model .
Specifically , we investigated the effects on motor dysfunction , microglial activation , and the loss of DA neurons .
Then , galangin was used to detect the impact on the inflammatory responses and inflammatory signaling pathways in LPS-induced BV-2 cells .
The in vivo results showed that galangin dose-dependently attenuates the activation of microglia , the loss of DA neurons , and motor dysfunction .
In vitro , @ @ @ @ @ @ @ necrosis factorα ( TNF-α ) , interleukin-6 ( IL-6 ) and interleukin-1β ( IL-1β ) , cyclooxygenase 2 ( COX-2 ) , and induced nitric oxide synthase ( iNOS ) via associating with the phosphorylation of c-JUN N-terminal Kinase ( JNK ) , p38 , protein kinase B ( AKT ) , and nuclear factor κB ( NF-κB ) p65 .
Collectively , the results indicated that galangin has a role in protecting DA neurons by inhibiting microglial activation .

Parkinson's disease (PD) is caused by the loss of dopaminergic (DA) neurons in the midbrain substantia nigra (SN). Neuroinflammation, which is marked by microglial activation, plays a very important role in the pathogenesis of PD. Pro-inflammatory mediators produced by activated microglia could damage DA neurons. Hence, the inhibition of microglial activation may provide a new approach for treating PD. Galangin has been shown to inhibit inflammation in a variety of diseases, but not PD. In this study, we aimed to investigate the anti-inflammatory effect of galangin and the underlying mechanisms in Lipopolysaccharide (LPS) induced PD models. We first examined the protective effect of galangin in the LPS-induced PD rat model. Specifically, we investigated the effects on motor dysfunction, microglial activation, and the loss of DA neurons. Then, galangin was used to detect the impact on the inflammatory responses and inflammatory signaling pathways in LPS-induced BV-2 cells. The in vivo results showed that galangin dose-dependently attenuates the activation of microglia, the loss of DA neurons, and motor dysfunction. In vitro, galangin markedly inhibited LPS-induced expression of tumor necrosis factorα (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β), cyclooxygenase 2 (COX-2), and induced nitric oxide synthase (iNOS) via associating with the phosphorylation of c-JUN N-terminal Kinase (JNK), p38, protein kinase B (AKT), and nuclear factor κB (NF-κB) p65. Collectively, the results indicated that galangin has a role in protecting DA neurons by inhibiting microglial activation.


greenmedinfo--2020-03-30--Galangin induces p53-independent S-phase arrest and apoptosis in human nasopharyngeal carcinoma cell

Galangin induces p53-independent S-phase arrest and apoptosis in human nasopharyngeal carcinoma cells.

BACKGROUND/AIM : Anti-cancer activity of 3,5,7-trihydroxyflavone ( galangin ) has been documented in a variety of cancer types ; however @ @ @ @ @ nasopharyngeal carcinoma ( NPC ) cells remains undetermined .
MATERIALS AND METHODS : Human NPC @ @ @ @ @ galangin .
Apoptosis was analyzed by assessing nuclear condensation , cleavage of pro-caspase-3 and poly @ @ @ @ @ , and DNA fragmentation .
Short hairpin RNA-mediated silencing of p53 was used for characterizing @ @ @ @ @ the anti-cancer activity of galangin .
Phosphatidylinositol 3-kinase ( PI3K ) inhibitor , protein kinase @ @ @ @ @ , and ectopic expression of wild type p85α or p85α mutant lacking p110α-binding ability were @ @ @ @ @ of PI3K/AKT inactivation in galangin-induced apoptosis .
RESULTS : Galangin induces apoptosis and S-phase arrest @ @ @ @ @ pathway .
Silencing of p53 did not block the anti-cancer activity of galangin on NPC @ @ @ @ @ effects on apoptosis and S-phase arrest in NPC cells are mediated via interfering with the @ @ @ @ @ p53-independent manner .

BACKGROUND/AIM: Anti-cancer activity of 3,5,7-trihydroxyflavone (galangin) has been documented in a variety of cancer types; however, its effect on human nasopharyngeal carcinoma (NPC) cells remains undetermined.
MATERIALS AND METHODS: Human NPC cell lines were treated with galangin. Apoptosis was analyzed by assessing nuclear condensation, cleavage of pro-caspase-3 and poly ADP-ribose polymerase (PARP), and DNA fragmentation. Short hairpin RNA-mediated silencing of p53 was used for characterizing the role of p53 in the anti-cancer activity of galangin. Phosphatidylinositol 3-kinase (PI3K) inhibitor, protein kinase B (AKT) inhibitor, and ectopic expression of wild type p85α or p85α mutant lacking p110α-binding ability were utilized to confirm the involvement of PI3K/AKT inactivation in galangin-induced apoptosis.
RESULTS: Galangin induces apoptosis and S-phase arrest by attenuating the PI3K/AKT signaling pathway. Silencing of p53 did not block the anti-cancer activity of galangin on NPC cells.
CONCLUSION: Galangin effects on apoptosis and S-phase arrest in NPC cells are mediated via interfering with the PI3K-AKT signaling pathway in a p53-independent manner.


greenmedinfo--2020-03-30--Two Plans To "Re-Open" the Country Include COVID-19 Tracking Via Cell Phones and Mass Vaccination Pr

Two Plans To "Re-Open" the Country Include COVID-19 Tracking Via Cell Phones and Mass Vaccination Program

As the world , and the United States , waits anxiously for news of when the outbreak and lockdown will end , two new plans outline requirements that will significantly impact our already suspended civil liberties .
An important article published in STAT titled , “ Two new road maps lay out possible paths to end coronavirus lockdowns , ” reveals two plans for re-opening our country , one which offers no definite timeline , and the second indicating the soonest would be June : Ezerkiel Emanuel is vice provost of global initiatives and a professor at the University of @ @ @ @ @ @ @ how to “ stop the virus ” is : “ A nationwide shelter-in-place or quarantine should take place for the next eight to 10 weeks .
According to Chinese data , this would mean the number of Covid-19 cases would peak in four weeks or so and then decline over the next four to six weeks .
So , as hard as it would be , everybody but essential workers would have to remain inside until roughly June 1st.
” Included in his suggestions are the following remedies , predicated as they are @ @ @ @ @ @ @ an egregious violation of privacy : • “ State and local health department then need to deploy thousands of teams to trace contacts of all new Covid-19 cases using cellphone data , social media data , and data from thermometer tests and the like .
We also need to get infected people to inform their own contacts .
It would be easier to lift the national quarantine if we isolate new cases , find and test all their contacts , and isolate any of them who may be infected.
” • “ Create @ @ @ @ @ @ @ use blood tests to certify people who have had Covid-19 , are immune and are no longer contagious .
These people could then work in hospitals or other areas where being risk-free would be a benefit.
” Emanuel 's mention of a `` Covid-19 certification system '' is reminiscient of the `` digital certificate '' s Bill Gates recently suggested would be requried to ensure that everyone has either been validated to have immunity to COVID or received a vaccine against it .
Gates also recently suggested that digital certificates of this kind @ @ @ @ @ @ @ future .
Emanuel estimated that if these , and additional steps are taken the earliest the national lockdown could lift is by June .
The timeline suggested by Emmanuel agrees with statements Trump delivered yesterday ( 3/30/20 ) , wherein he said that he believed cases of COVID-19 would peak by Easter , and that a recovery would begin in June .
Gotleib 's Plan With Plenty of Conditions , But No Definite Timeline The second , 20-page plan was devised by Scott Gotleib who is a former commissioner of the FDA , @ @ @ @ @ @ @ Pfizer ; Gotleib , along with several co-authors , including Caitlin Rivers , an assistant professor of epidemiology at the Johns Hopkins Center for Health Security , envisions four phases for re-opening the country .
Phase 1 : the current situation , in which the outbreak is growing .
Phase 2 : this phase begins when certain conditions are met -- such as hospitals being able to handle the influx of new incoming cases , and new cases have dropped for at least 14 days .
The report suggests that if containment erodes @ @ @ @ @ @ @ would fall back to Phase 1 status .
Phase 3 : the lifting of all restrictions would only occur when a vaccine and therapeutics are available , which Gottlieb estimates would take two years away for the vaccine , and sooner for medications ( by summer ) .
Phase 4 : would involve building the country ’ s capacity to respond to the next biological threat .
Gottleib 's plan like also suggests utilizing highly invasive surveillance of the population via the GPS functionality of cell phones : '' Massively Scale Contact Tracing @ @ @ @ @ @ @ new case of COVID-19 is diagnosed , the patient should be isolated either at home or in a hospital , depending on the level of care he or she requires .
Current CDC guidelines recommend seven days of isolation.15 Home isolation can be enforced using technology such as GPS tracking on cell phone apps .
Also , the close contacts of confirmed cases ( as defined by the CDC16 ) should be quarantined and monitored daily for 14 days .
Monitoring of international travelers is also recommended . ''
Gottleib 's plan also @ @ @ @ @ @ @ vaccination program in anticipation of the availability of a COVID-19 vaccine : Gottleib 's plan offers no definitive timeline ; rather , the prospect of the lifting of quarantines and socio-economic restrictions is pegged to whether or not people comply with its directives .
In essence , the nation 's economy is being held hostage by a plan which would require the indefinite suspension of a number of civil liberties , and only a theoretical promise that a future vaccine and/or pharmaceutical combination would make a significant impact on the outbreak , before @ @ @ @ @ @ @ to normal . ''
Given the immediate adverse impacts that social distancing , such as the closing of millions of businesses , has on the health and well-being of countless affected individuals , it is difficult to understand how these plans ignore other very real causes of mortality ( see image below ) -- some of which are known to greatly increase due to the stress and socioeconomic impacts restrictions like these have .
Please join Stand for Health Freedom to learn what you can do to maintain your civil liberties and health @ @ @ @ @ @

Visit our Re-post guidelines This article is copyrighted by GreenMedInfo LLC, 2020
As the world, and the United States, waits anxiously for news of when the outbreak and lockdown will end, two new plans outline requirements that will significantly impact our already suspended civil liberties.
An important article published in STAT titled, “Two new road maps lay out possible paths to end coronavirus lockdowns,” reveals two plans for re-opening our country, one which offers no definite timeline, and the second indicating the soonest would be June:
“The first, from Ezekiel Emanuel, a health policy expert and vice-provost of the University of Pennsylvania, suggests lockdowns could ease up in June. The second, from former Food and Drug Administration commissioner Scott Gottlieb and colleagues, doesn’t set a date, but rather outlines the evidence that communities would need to begin lifting some of the more draconian restrictions.”
Ezekiel Emanuel is vice provost of global initiatives and a professor at the University of Pennsylvania. Emanuel’s opinion on how to “stop the virus” is:
“A nationwide shelter-in-place or quarantine should take place for the next eight to 10 weeks. According to Chinese data, this would mean the number of Covid-19 cases would peak in four weeks or so and then decline over the next four to six weeks. So, as hard as it would be, everybody but essential workers would have to remain inside until roughly June 1st.”
Included in his suggestions are the following remedies, predicated as they are on surveillance of the entire population and an egregious violation of privacy:
“ State and local health department then need to deploy thousands of teams to trace contacts of all new Covid-19 cases using cellphone data, social media data, and data from thermometer tests and the like. We also need to get infected people to inform their own contacts. It would be easier to lift the national quarantine if we isolate new cases, find and test all their contacts, and isolate any of them who may be infected.”
“Create a Covid-19 certification system. States should use blood tests to certify people who have had Covid-19, are immune and are no longer contagious. These people could then work in hospitals or other areas where being risk-free would be a benefit.”
Emanuel's mention of a "Covid-19 certification system" is reminiscient of the "digital certificate"s Bill Gates recently suggested would be requried to ensure that everyone has either been validated to have immunity to COVID or received a vaccine against it. Gates also recently suggested that digital certificates of this kind would be required to travel in the future.
Emanuel estimated that if these, and additional steps are taken the earliest the national lockdown could lift is by June. The timeline suggested by Emmanuel agrees with statements Trump delivered yesterday (3/30/20), wherein he said that he believed cases of COVID-19 would peak by Easter, and that a recovery would begin in June.
Gotleib's Plan With Plenty of Conditions, But No Definite Timeline
The second, 20-page plan was devised by Scott Gotleib who is a former commissioner of the FDA, and actively sits on the board of Pfizer; Gotleib, along with several co-authors, including Caitlin Rivers, an assistant professor of epidemiology at the Johns Hopkins Center for Health Security, envisions four phases for re-opening the country.
Phase 1: the current situation, in which the outbreak is growing.
Phase 2: this phase begins when certain conditions are met -- such as hospitals being able to handle the influx of new incoming cases, and new cases have dropped for at least 14 days. The report suggests that if containment erodes in specific counties or states, they would fall back to Phase 1 status.
Phase 3: the lifting of all restrictions would only occur when a vaccine and therapeutics are available, which Gottlieb estimates would take two years away for the vaccine, and sooner for medications (by summer).
Phase 4: would involve building the country’s capacity to respond to the next biological threat.
Gottleib's plan like also suggests utilizing highly invasive surveillance of the population via the GPS functionality of cell phones:
"Massively Scale Contact Tracing and Isolation and Quarantine. When a new case of COVID-19 is diagnosed, the patient should be isolated either at home or in a hospital, depending on the level of care he or she requires. Current CDC guidelines recommend seven days of isolation.15 Home isolation can be enforced using technology such as GPS tracking on cell phone apps. Also, the close contacts of confirmed cases (as defined by the CDC16) should be quarantined and monitored daily for 14 days. Monitoring of international travelers is also recommended."
Gottleib's plan also calls for the development of a mass vaccination program in anticipation of the availability of a COVID-19 vaccine:
"Trigger for Switch Toward Mass Vaccination. Once availability of a vaccine or therapeutic is able to meet demand, vaccination can expand beyond priority groups. The CDC, state public-health agencies, and vaccine developers should work together to plan for and execute mass vaccination of large populations in the US. This planning can begin before Phase III because preparation can be made regardless of vaccine availability."
Gottleib's plan offers no definitive timeline; rather, the prospect of the lifting of quarantines and socio-economic restrictions is pegged to whether or not people comply with its directives. In essence, the nation's economy is being held hostage by a plan which would require the indefinite suspension of a number of civil liberties, and only a theoretical promise that a future vaccine and/or pharmaceutical combination would make a significant impact on the outbreak, before things are allowed to "go back to normal." Given the immediate adverse impacts that social distancing, such as the closing of millions of businesses, has on the health and well-being of countless affected individuals, it is difficult to understand how these plans ignore other very real causes of mortality (see image below) -- some of which are known to greatly increase due to the stress and socioeconomic impacts restrictions like these have.
Please join Stand for Health Freedom to learn what you can do to maintain your civil liberties and health freedom in these difficult times.


greenmedinfo--2020-03-30--Galangin could suppress the viability of MCF-7 cells and induce cell apoptosis.

AIMS : The study aimed to investigate the molecular mechanism of inhibition of proliferation and apoptosis induction by galangin against MCF-7 human breast cancer cells .
METHODS : Cell Counting Kit-8 assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis .
The expression level of apoptosis-related proteins ( cleaved-caspase-9 , cleaved-caspase-8 , cleaved-caspase-3 , Bad , cleaved-Bid , Bcl-2 , Bax , p-phosphatidylinositol 3-kinase [ PI3K ] , and p-Akt ) and cell cycle-related proteins ( cyclin D3 , cyclin B1 , cyclin-dependent kinases CDK1 , CDK2 , CDK4 , p21 , p27 @ @ @ @ @ @ @ blotting .
RESULTS : Galangin increased the expression of Bax and decreased the expression of Bcl-2 in a concentration-dependent manner , inhibited cell viability , and induced apoptosis .
Meanwhile , the expression of cleavage of caspase-9 , caspase-8 , caspase-3 , Bid , and Bad increased significantly while the expression of p-PI3K and p-Akt proteins decreased .
In addition , the protein levels of cyclin D3 , cyclin B1 , CDK1 , CDK2 , and CDK4 were downregulated while the expression levels of p21 , p27 , and p53 were upregulated significantly @ @ @ @ @ @ @ viability of MCF-7 cells and induce cell apoptosis via the mitochondrial pathway and PI3K/Akt inhibition as well as cell cycle arrest .

AIMS: The study aimed to investigate the molecular mechanism of inhibition of proliferation and apoptosis induction by galangin against MCF-7 human breast cancer cells.
METHODS: Cell Counting Kit-8 assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis. The expression level of apoptosis-related proteins (cleaved-caspase-9, cleaved-caspase-8, cleaved-caspase-3, Bad, cleaved-Bid, Bcl-2, Bax, p-phosphatidylinositol 3-kinase [PI3K], and p-Akt) and cell cycle-related proteins (cyclin D3, cyclin B1, cyclin-dependent kinases CDK1, CDK2, CDK4, p21, p27, p53) were evaluated by Western blotting.
RESULTS: Galangin increased the expression of Bax and decreased the expression of Bcl-2 in a concentration-dependent manner, inhibited cell viability, and induced apoptosis. Meanwhile, the expression of cleavage of caspase-9, caspase-8, caspase-3, Bid, and Bad increased significantly while the expression of p-PI3K and p-Akt proteins decreased. In addition, the protein levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated while the expression levels of p21, p27, and p53 were upregulated significantly.
CONCLUSION: Galangin could suppress the viability of MCF-7 cells and induce cell apoptosis via the mitochondrial pathway and PI3K/Akt inhibition as well as cell cycle arrest.


greenmedinfo--2020-03-30--Administration of galangin reduced hyperlipidaemia related to the risk of diabetic complications.

CONTEXT : Galangin , a natural flavonoid , is found in honey and Alpinia officinarum Hance ( Zingiberaceae ) .
@ @ @ @ @ , antidiabetic and anticancer properties , without side effects .
The effects of galangin on @ @ @ @ @ not known .
OBJECTIVE : To elucidate the effectiveness of galangin on hyperglycaemia-associated complications and @ @ @ @ @ streptozotocin ( STZ ) -induced hyperglycaemia .
MATERIALS AND METHODS : Diabetes was induced in @ @ @ @ @ 40 mg/kg of STZ .
In our previous study , galangin had no toxicity at @ @ @ @ @ .
Therefore three doses of galangin ( 4 , 8 or 16 mg/kg BW ) @ @ @ @ @ BW ) were administered daily to diabetic rats orally for 45 days .
DISCUSSION AND @ @ @ @ @ reduced hyperlipidaemia related to the risk of diabetic complications and could be beneficial for diabetic @ @ @ @ @ detailing its mechanism-of-action for improving hyperglycaemic-associated lipid abnormalities is needed .

CONTEXT: Galangin, a natural flavonoid, is found in honey and Alpinia officinarum Hance (Zingiberaceae). Galangin has antiviral, antimicrobial, antidiabetic and anticancer properties, without side effects. The effects of galangin on hyperglycaemia and lipid abnormalities are not known.
OBJECTIVE: To elucidate the effectiveness of galangin on hyperglycaemia-associated complications and lipid changes in rats with streptozotocin (STZ)-induced hyperglycaemia.
MATERIALS AND METHODS: Diabetes was induced in adult Wistar rats by administering 40 mg/kg of STZ. In our previous study, galangin had no toxicity at concentrations up to 320 mg/kg. Therefore three doses of galangin (4, 8 or 16 mg/kg BW) or glibenclamide (600 µg/kg BW) were administered daily to diabetic rats orally for 45 days.
RESULTS: Diabetic rats showed a significant (p < 0.05) increased levels of plasma glucose (281.10 mg/dL) and decreased levels of insulin (6.01 μU/mL). Additionally, diabetic rats showed a significant (p < 0.05) increased levels of plasma lipid profiles such as total cholesterol (149.05 mg/dL), triglycerides (143.28 mg/dL), free fatty acids (139.37 mg/dL), phospholipids (127.53 mg/dL), plasma low-density lipoprotein-cholesterol (98.72 mg/dL), plasma very low-density lipoprotein-cholesterol (28.65 mg/dL), and significant (p < 0.05) decreased in plasma high-density lipoprotein-cholesterol (21.68 mg/dL). When galangin was administered to the hyperglycaemic rats, plasma glucose and insulin levels and lipid profiles reverted to levels similar to those in healthy control rats.
DISCUSSION AND CONCLUSIONS: Administration of galangin reduced hyperlipidaemia related to the risk of diabetic complications and could be beneficial for diabetic hyperlipidaemic patients. Further work detailing its mechanism-of-action for improving hyperglycaemic-associated lipid abnormalities is needed.


greenmedinfo--2020-03-30--Galangin inhibited lipopolysaccharide-induced neuroinflammation.

Neuroinflammation resulting from microglial activation is involved in the pathogenesis of neurodegenerative diseases , including Parkinson 's diseases .
Microglial @ @ @ @ @ in neuroinflammation and contributes to several neurological disorders .
Hence , inhibition of both microglial @ @ @ @ @ pro-inflammatory cytokines may lead to an effective treatment for neurodegenerative diseases .
In the present @ @ @ @ @ of galangin were investigated in lipopolysaccharide ( LPS ) -stimulated BV-2 microglial cells .
Galangin @ @ @ @ @ nitric oxide , interleukin-1β , and inducible nitric oxide synthase in LPS-stimulated BV-2 microglial cells @ @ @ @ @ inhibited the phosphorylation of p38 mitogen-activated protein kinase ( MAPK ) and c-Jun N-terminal kinase @ @ @ @ @ was observed that activation of both IκB-α and nuclear factor kappa B ( NF-κB ) @ @ @ @ @ stimulation , and this effect was suppressed by galangin treatment .
In conclusion , galangin @ @ @ @ @ LPS-stimulated BV-2 microglial cells .
Galangin inhibited LPS-induced neuroinflammation via the MAPK and NF-κB signaling @ @ @ @ @ a natural therapeutic agent for the treatment of various neuroinflammatory conditions .

Neuroinflammation resulting from microglial activation is involved in the pathogenesis of neurodegenerative diseases, including Parkinson's diseases. Microglial activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglial activation and the generation of pro-inflammatory cytokines may lead to an effective treatment for neurodegenerative diseases. In the present study, the anti-neuroinflammatory effects of galangin were investigated in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Galangin significantly decreased the generation of nitric oxide, interleukin-1β, and inducible nitric oxide synthase in LPS-stimulated BV-2 microglial cells. In addition, galangin inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase 1/2. Furthermore, it was observed that activation of both IκB-α and nuclear factor kappa B(NF-κB) was significantly increased following LPS stimulation, and this effect was suppressed by galangin treatment. In conclusion, galangin displayed an anti-neuroinflammatory activity in LPS-stimulated BV-2 microglial cells. Galangin inhibited LPS-induced neuroinflammation via the MAPK and NF-κB signaling pathways and might act as a natural therapeutic agent for the treatment of various neuroinflammatory conditions.


greenmedinfo--2020-03-30--Galangin could prove a useful new molecule in the treatment of kidney carcinoma.

PURPOSE : Galangin is an important flavonoid that has been reported to be of immense pharmacological importance .
It has been shown to have a number of bioactivities which range from anticancer to antimicrobial .
In this study the effects of Galangin were studied on the proliferation of the A498 kidney cancer cells .
METHODS : The antiproliferative effects were tested by MTT assay .
Apoptosis was checked by subjecting the A498 cell to DAPI and annexin V/PI double staining .
The effect on the cell migration and invasion was assessed by Boyden chamber assays .
The expression of the @ @ @ @ @ @ @ analysis .
RESULTS : Galangin inhibited the proliferation of the kidney cancer A498 cells .
The IC50 of Galangin against the A498 cancer cells was 15μM .
The anticancer effects of Galangin were due to induction of apoptosis in the A498 cancer cells as indicated by DAPI and annexin V/PI staining .
Furthermore , Galangin could increase the expression of Bax , Cyt-c and decrease the expression of Bcl-2 .
Galangin could also inhibit the migration and invasion of the kidney cancer cells and also suppress the expression of some of the important @ @ @ @ @ @ @ CONCLUSION : In conclusion , Galangin could prove a useful new molecule in the treatment of kidney carcinoma .

PURPOSE: Galangin is an important flavonoid that has been reported to be of immense pharmacological importance. It has been shown to have a number of bioactivities which range from anticancer to antimicrobial. In this study the effects of Galangin were studied on the proliferation of the A498 kidney cancer cells.
METHODS: The antiproliferative effects were tested by MTT assay. Apoptosis was checked by subjecting the A498 cell to DAPI and annexin V/PI double staining. The effect on the cell migration and invasion was assessed by Boyden chamber assays. The expression of the apoptosis-related proteins was examined by western blot analysis.
RESULTS: Galangin inhibited the proliferation of the kidney cancer A498 cells. The IC50 of Galangin against the A498 cancer cells was 15μM. The anticancer effects of Galangin were due to induction of apoptosis in the A498 cancer cells as indicated by DAPI and annexin V/PI staining. Furthermore, Galangin could increase the expression of Bax, Cyt-c and decrease the expression of Bcl-2. Galangin could also inhibit the migration and invasion of the kidney cancer cells and also suppress the expression of some of the important proteins of the PI3K/AKT/mTOR signalling pathway.
CONCLUSION: In conclusion, Galangin could prove a useful new molecule in the treatment of kidney carcinoma.


greenmedinfo--2020-03-30--Galangin inhibits α-glucosidase activity and formation of non-enzymatic glycation products.

Inhibition ofα-glucosidase and non-enzymatic glycation is considered as an effective approach to treat type 2 diabetes .
Herein , multispectroscopic @ @ @ @ @ were used to investigate the inhibition of galangin on α-glucosidase and non-enzymatic glycation .
Galangin @ @ @ @ @ α-glucosidase activity in a mixed-type manner through a monophasic kinetic process , and induced the @ @ @ @ @ of α-glucosidase by forming α-glucosidase-galgangin complex .
Molecular docking revealed that galangin primarily interacted withthe @ @ @ @ @ active site of α-glucosidase , which may prevent the entrance of substrate resulting in a @ @ @ @ @ α-glucosidase .
Moreover , galangin moderately inhibited the formation of intermediates of non-enzymatic glycation , @ @ @ @ @ strongly inhibited the formation of advanced glycation end products .

Inhibition ofα-glucosidase and non-enzymatic glycation is considered as an effective approach to treat type 2 diabetes. Herein, multispectroscopic techniques and molecular docking analysis were used to investigate the inhibition of galangin on α-glucosidase and non-enzymatic glycation. Galangin showed a reversible inhibition on α-glucosidase activity in a mixed-type manner through a monophasic kinetic process, and induced the fluorescence quenching and conformational changes of α-glucosidase by forming α-glucosidase-galgangin complex. Molecular docking revealed that galangin primarily interacted withthe amino acid residues within the active site of α-glucosidase, which may prevent the entrance of substrate resulting in a decrease in catalytic efficiency of α-glucosidase. Moreover, galangin moderately inhibited the formation of intermediates of non-enzymatic glycation, fructosamine and α-dicarbonyl compounds and strongly inhibited the formation of advanced glycation end products.


greenmedinfo--2020-03-30--Galangin alleviates liver ischemia-reperfusion injury.

BACKGROUND/AIMS : Liver ischemia-reperfusion ( I/R ) injury is a pathological process that often occurs during liver and trauma surgery .
There are numerous causes of liver I/R injury , but the mechanism is unknown .
Galangin ( GA ) is a flavonoid , a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory , antioxidant , and antitumor activity .
This study evaluated the protective effect of GA on hepatic I/R injury .
METHODS : An I/R model was created in male Wistar rats by clamping the hepatoportal vein , hepatic artery and hepatic duct for 30 min @ @ @ @ @ @ @ hypoxia/restoration ( H/R ) model was established in buffalo rat liver ( BRL ) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST , hepatic histology , and MPO activity .
Oxidative stress was assayed by serum superoxide dismutase ( SOD ) , catalase ( CAT ) , glutathione ( GSH ) and malondialdehyde ( MDA ) .
Expression of apoptosis-related proteins in BRL cells was assayed in western blots .
Expression of AKT and p-AKT proteins in vivo @ @ @ @ @ @ @ .
RESULTS : GA significantly decreased ALT/AST expression , reversed changes in oxidative stress markers induced by I/R , and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro .
Methylthiazol tetrazolium ( MTT ) assay , flow cytometry , and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells .
GA also increased the expression of phosphorylated AKT after H/R .
CONCLUSION : GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis .
PI3K/AKT signaling have been involved .
GA may @ @ @ @ @ @ @ potential therapeutic candidate .

BACKGROUND/AIMS: Liver ischemia-reperfusion (I/R) injury is a pathological process that often occurs during liver and trauma surgery. There are numerous causes of liver I/R injury, but the mechanism is unknown. Galangin (GA) is a flavonoid, a polyphenolic compound widely distributed in medicinal herbs that has anti-inflammatory, antioxidant, and antitumor activity. This study evaluated the protective effect of GA on hepatic I/R injury.
METHODS: An I/R model was created in male Wistar rats by clamping the hepatoportal vein, hepatic artery and hepatic duct for 30 min followed by reperfusion for 2 h. A hypoxia/restoration (H/R) model was established in buffalo rat liver (BRL) cells by hypoxia for 4 h followed by normoxic conditions for 10 h. The extent of liver injury was assayed by serum ALT/AST, hepatic histology, and MPO activity. Oxidative stress was assayed by serum superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondialdehyde (MDA). Expression of apoptosis-related proteins in BRL cells was assayed in western blots. Expression of AKT and p-AKT proteins in vivo and vitro were assayed in western blots.
RESULTS: GA significantly decreased ALT/AST expression, reversed changes in oxidative stress markers induced by I/R, and mediated caspase-3 activity expression of apoptosis-related proteins in vivo and in vitro. Methylthiazol tetrazolium (MTT) assay, flow cytometry, and Hoechst 33258 staining confirmed that GA inhibited apoptosis of BRL cells. GA also increased the expression of phosphorylated AKT after H/R.
CONCLUSION: GA reduced liver I/R injury both in vivo and vitro and inhibited BRL cell apoptosis. PI3K/AKT signaling have been involved. GA may protect against liver I/R and be a potential therapeutic candidate.


greenmedinfo--2020-03-30--Chemopreventive mechanisms of galangin against hepatocellular carcinoma.

Hepatocellular carcinoma ( HCC ) is one of the most common cancers and has a high mortality rate in less developed countries , especially in China .
Galangin ( GA ) , one of the most important and naturally active flavonoids , extracted primarily from the root of Alpinia officinarum Hance , has been demonstrated to be effective in the treatment of HCC .
It is a substance with defensive actions and a broad range of biological properties , including inhibitory effects on bacteria , fungi , viruses , the control of hypertension and diabetes , and chemoprevention of several @ @ @ @ @ @ @ prevents HCC through multiple anti-cancer mechanisms , anti-genotoxic activity against environmental and dietary carcinogens ; anti-proliferative effects through reversal of the Warburg effect in HCC ; arrest of the cell cycle in the G0/G1 phase ; induction of apoptosis via stimulation of reactive oxygen species ( ROS ) , endoplasmic reticulum ( ER ) stress , and the mitochondrial-dependent apoptosis pathway ; induction of autophagy ; and inhibition of angiogenesis , metastasis , and multidrug resistance ( MDR ) .
In addition , synergistic effects with other chemotherapy drugs have been demonstrated .
@ @ @ @ @ @ @ the anti-HCC mechanisms of GA .

Hepatocellular carcinoma (HCC) is one of the most common cancers and has a high mortality rate in less developed countries, especially in China. Galangin (GA), one of the most important and naturally active flavonoids, extracted primarily from the root of Alpinia officinarum Hance, has been demonstrated to be effective in the treatment of HCC. It is a substance with defensive actions and a broad range of biological properties, including inhibitory effects on bacteria, fungi, viruses, the control of hypertension and diabetes, and chemoprevention of several cancers. Experiments have shown that GA prevents HCC through multiple anti-cancer mechanisms, anti-genotoxic activity against environmental and dietary carcinogens; anti-proliferative effects through reversal of the Warburg effect in HCC; arrest of the cell cycle in the G0/G1 phase; induction of apoptosis via stimulation of reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and the mitochondrial-dependent apoptosis pathway; induction of autophagy; and inhibition of angiogenesis, metastasis, and multidrug resistance (MDR). In addition, synergistic effects with other chemotherapy drugs have been demonstrated. Therefore, this review is focused on the anti-HCC mechanisms of GA.


greenmedinfo--2020-03-30--Galangin prevents increased susceptibility to pentylenetetrazol-stimulated seizures by prostaglandin

Galangin prevents increased susceptibility to pentylenetetrazol-stimulated seizures by prostaglandin E2.

Epilepsy is one of the most common chronic neurological diseases .
It is characterized by recurrent epileptic seizures , where one-third of patients are refractory to existing treatments .
Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators , such as prostaglandin E ( PGE ) , during seizures .
The purpose of this study was to investigate whether PGEincreases susceptibility to pentylenetetrazol-induced ( PTZ ) seizures .
Subsequently , we evaluated if the flavonoid isolated from the plant Piper aleyreanum ( galangin ) presented @ @ @ @ @ @ @ that the group treated with PGEincreased susceptibility to PTZ and caused myoclonic and generalized seizures , which increased seizure duration and electroencephalographic wave amplitudes .
Furthermore , treatment with PGEand PTZ increased IBA-1 ( microglial marker ) , GFAP ( astrocytic marker ) , 4-HNE ( lipid peroxidation marker ) , VCAM-1 ( vascular cell adhesion molecule 1 ) , and p-PKAIIα ( phosphorylated cAMP-dependent protein kinase ) immunocontent .
Indeed , galangin prevented behavioral and electroencephalographic seizures , reactive species production , decreased microglial and astrocytic immunocontent , as well as decreased @ @ @ @ @ @ @ PGE/PTZ .
Therefore , this study suggests galangin may have an antagonizing role on PGE-induced effects , reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGEand PTZ .
However , further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms .

Epilepsy is one of the most common chronic neurological diseases. It is characterized by recurrent epileptic seizures, where one-third of patients are refractory to existing treatments. Evidence revealed the association between neuroinflammation and increased susceptibility to seizures since there is a pronounced increase in the expression of key inflammatory mediators, such as prostaglandin E(PGE), during seizures. The purpose of this study was to investigate whether PGEincreases susceptibility to pentylenetetrazol-induced (PTZ) seizures. Subsequently, we evaluated if the flavonoid isolated from the plant Piper aleyreanum (galangin) presented any anticonvulsive effects. Our results demonstrated that the group treated with PGEincreased susceptibility to PTZ and caused myoclonic and generalized seizures, which increased seizure duration and electroencephalographic wave amplitudes. Furthermore, treatment with PGEand PTZ increased IBA-1 (microglial marker), GFAP (astrocytic marker), 4-HNE (lipid peroxidation marker), VCAM-1 (vascular cell adhesion molecule 1), and p-PKAIIα (phosphorylated cAMP-dependent protein kinase) immunocontent. Indeed, galangin prevented behavioral and electroencephalographic seizures, reactive species production, decreased microglial and astrocytic immunocontent, as well as decreased VCAM-1 immunocontent and p-PKA/PKA ratio induced by PGE/PTZ. Therefore, this study suggests galangin may have an antagonizing role on PGE-induced effects, reducing cerebral inflammation and protecting from excitatory effects evidenced by administrating PGEand PTZ. However, further studies are needed to investigate the clinical implications of the findings and their underlying mechanisms.


greenmedinfo--2020-03-30--Galangin might represent a promising adjuvant therapy to prevent hepatotoxicity in patients on cyclo

Galangin might represent a promising adjuvant therapy to prevent hepatotoxicity in patients on cyclophosphamide treatment.

Cyclophosphamide ( CP ) is a widely used chemotherapeutic agent ; however , its clinical application is limited because of its multi-organ toxicity .
Galangin ( Gal ) is a bioactive flavonoid with promising biological activities .
This study investigated the hepatoprotective effect of Gal in CP-induced rats .
Rats received Gal ( 15 , 30 and 60 mg/kg/day ) for 15 days followed by a single dose of CP at day 16 .
Cyclophosphamide triggered liver injury characterized by elevated serum transaminases , alkaline phosphatase ( ALP ) and lactate dehydrogenase ( LDH ) , and histopathological manifestations .
@ @ @ @ @ @ @ , nitric oxide , and oxidative DNA damage along with declined glutathione and antioxidant enzymes were demonstrated in CP-administered rats .
CP provoked hepatic nuclear factor-kappaB ( NF-κB ) phosphorylation and increased mRNA abundance of inducible nitric oxide synthase ( iNOS ) and cyclooxygenase-2 ( COX-2 ) , and tumor necrosis factor-alpha ( TNF-α ) and interleukin-1 beta ( IL-1β ) both expression and serum levels .
Gal prevented CP-induced liver injury , boosted antioxidants and suppressed oxidative stress , DNA damage , NF-κB phosphorylation and pro-inflammatory mediators .
Gal diminished Bax and @ @ @ @ @ @ @ Bcl-2 ) in liver of CP-administered rats .
In addition , Gal increased peroxisome proliferator-activated receptor gamma ( PPARγ ) expression and activated hepatic nuclear factor erythroid 2-related factor 2 ( Nrf2 ) signaling showed by the increase in Nrf2 , NAD ( P ) H : quinone acceptor oxidoreductase-1 ( NQO-1 ) and heme oxygenase 1 ( HO-1 ) in CP-administered rats .
These findings suggest that Gal prevents CP hepatotoxicity through activation of Nrf2/HO-1 signaling and attenuation of oxidative damage , inflammation and cell death .
Therefore , Gal might represent @ @ @ @ @ @ @ in patients on CP treatment .

Cyclophosphamide (CP) is a widely used chemotherapeutic agent; however, its clinical application is limited because of its multi-organ toxicity. Galangin (Gal) is a bioactive flavonoid with promising biological activities. This study investigated the hepatoprotective effect of Gal in CP-induced rats. Rats received Gal (15, 30 and 60 mg/kg/day) for 15 days followed by a single dose of CP at day 16. Cyclophosphamide triggered liver injury characterized by elevated serum transaminases, alkaline phosphatase (ALP) and lactate dehydrogenase (LDH), and histopathological manifestations. Increased hepatic reactive oxygen species, malondialdehyde, nitric oxide, and oxidative DNA damage along with declined glutathione and antioxidant enzymes were demonstrated in CP-administered rats. CP provoked hepatic nuclear factor-kappaB (NF-κB) phosphorylation and increased mRNA abundance of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) both expression and serum levels. Gal prevented CP-induced liver injury, boosted antioxidants and suppressed oxidative stress, DNA damage, NF-κB phosphorylation and pro-inflammatory mediators. Gal diminished Bax and caspase-3, and increased B-cell lymphoma-2 (Bcl-2) in liver of CP-administered rats. In addition, Gal increased peroxisome proliferator-activated receptor gamma (PPARγ) expression and activated hepatic nuclear factor erythroid 2-related factor 2 (Nrf2) signaling showed by the increase in Nrf2, NAD(P)H: quinone acceptor oxidoreductase-1 (NQO-1) and heme oxygenase 1 (HO-1) in CP-administered rats. These findings suggest that Gal prevents CP hepatotoxicity through activation of Nrf2/HO-1 signaling and attenuation of oxidative damage, inflammation and cell death. Therefore, Gal might represent a promising adjuvant therapy to prevent hepatotoxicity in patients on CP treatment.


greenmedinfo--2020-03-30--The natural flavonoid galangin ameliorates dextran sulphate sodium-induced ulcerative colitis.

This study was carried out to investigate the potential therapeutic effect of galangin , a promising active principle of honeybee @ @ @ @ @ sodium ( DSS ) -induced colitis in mice .
We explored the possible underlying mechanisms @ @ @ @ @ therapeutic benefit of adding galangin to the standard therapy sulphasalazine .
A galangin dose of @ @ @ @ @ on a preliminary dose-selection study for investigation in a 4-week cyclical model of DSS-induced colitis @ @ @ @ @ DSS in their drinking water during the first and third weeks and were administered the @ @ @ @ @ , 100 mg/kg sulphasalazine anda combination of 20 mg/kg galangin and 50 mg/kg sulphasalazine ) @ @ @ @ @ week .
Galangin significantly ameliorated DSS-induced histopathological alterations and tissue injury , down-regulated Toll-like receptor @ @ @ @ @ p65 activation , lowered inflammatory cytokine levels and demonstrated antioxidant effects .
The combination of @ @ @ @ @ doses yielded comparable results to either drug alone at full dose .
This study highlights @ @ @ @ @ for colitis management .

This study was carried out to investigate the potential therapeutic effect of galangin, a promising active principle of honeybee propolis, in dextran sulphate sodium (DSS)-induced colitis in mice. We explored the possible underlying mechanisms for galangin action and the therapeutic benefit of adding galangin to the standard therapy sulphasalazine. A galangin dose of 40 mg/kg was selected based on a preliminary dose-selection study for investigation in a 4-week cyclical model of DSS-induced colitis. Mice received 3% DSS in their drinking water during the first and third weeks and were administered the treatments (40 mg/kg galangin, 100 mg/kg sulphasalazine anda combination of 20 mg/kg galangin and 50 mg/kg sulphasalazine) daily starting from the second week. Galangin significantly ameliorated DSS-induced histopathological alterations and tissue injury, down-regulated Toll-like receptor 4 expression, suppressed NF-κB p65 activation, lowered inflammatory cytokine levels and demonstrated antioxidant effects. The combination of galangin and sulphasalazine at half doses yielded comparable results to either drug alone at full dose. This study highlights galangin as a promising therapy for colitis management.


greenmedinfo--2020-03-30--Propolis and olive leaf extract alone and in combinations with acyclovir have antiviral efficacy aga

Propolis and olive leaf extract alone and in combinations with acyclovir have antiviral efficacy against HSV-1.

While acyclovir , a nucleoside analogue , is widely used for herpes simplex virus type 1 ( HSV-1 ) , emergence of drug-resistant viruses due to frequent usage of this class of medicines , and their toxic side effects require exploring novel active molecules .
Despite the studies on developing synthetic molecules in medical sciences and pharmacology , herbs as a natural source of biologically-active compounds remain popular .
In this in vitro study , olive leaf extract ( OLE ) and propolis alone or in combination with acyclovir were investigated for their antiviral efficacy in HSV-1.Toxic doses of OLE @ @ @ @ @ @ @ propolis diluent , for Hep-2 ( ATCC , CCL-23 ) cells were determined by conventional cell culture .
Using '' endpoint '' method , the viral dose infecting half of the cell culture ( TCID50 ) was calculated , and viral quantity was determined with Spearman-Karber method .
Antiviral effects of OLE and propolis on HSV-1 were investigated by conventional cell culture and real-time cell analysis ( RTCA ) .
Combinations of the two extracts with one another and with acyclovir were evaluated by RTCA .
Active substances prepared at three different dilutions @ @ @ @ @ @ @ logTCID50 : 11.5 in descending order starting from the highest non-toxic concentration , and they were left at room temperature for two different durations ( one hour and three hours ) .
The aliquots taken from the tubes were cultured in plates containing Hep-2 cells and evaluated after 72 hours .
Combinations of extracts and acyclovir at concentrations at least four times lower than the lowest concentration showing antiviral efficacy against HSV-1 were cultured with Hep-2 cells in the e-plates of the xCELLigence RTCA device , measurements were obtained at 30 minute intervals @ @ @ @ @ @ @ time .
In the test with two different durations and at different concentrations of OLE and propolis , antiviral efficacy was observed both with one-hour and three-hour incubation at a concentration of 10μg/ ml for propolis and 1.2 mg/ml for OLE with RTCA .
The duration and concentration of the greatest decrease in viral quantity were in the first one hour and 10 μg/ml for propolis , and in the first one hour and 1.2 mg/ ml for OLE .
Combination of propolis and OLE with acyclovir caused no cytopathiceffects , and the @ @ @ @ @ @ @ effect .
According to these results , propolis and OLE , alone and in combinations with acyclovir , have antiviral efficacy against HSV-1 .
These agents may reduce the dose and side effects of acyclovir in case of co-administration sincethey exert their effects through a different mechanism than acyclovir , possibly through direct virucidal activity , inhibition of virus internalization or viral inhibition in early stages of replication ( inhibition of adsorption/binding of viral particles to the cell ) .
These extracts that do not require conversion to active form have the potential @ @ @ @ @ @ @ prevent spread , and be used in the topical treatment of acyclovir-resistant HSV infections , particularly in immunocompromised patients .
However , in vivo studies should be conducted to determine their medicinal properties and potential toxicities .
These results should be supported by further comprehensive studies and the efficacy against other viruses should also be investigated .

While acyclovir, a nucleoside analogue, is widely used for herpes simplex virus type 1 (HSV-1), emergence of drug-resistant viruses due to frequent usage of this class of medicines, and their toxic side effects require exploring novel active molecules. Despite the studies on developing synthetic molecules in medical sciences and pharmacology, herbs as a natural source of biologically-active compounds remain popular. In this in vitro study, olive leaf extract (OLE) and propolis alone or in combination with acyclovir were investigated for their antiviral efficacy in HSV-1.Toxic doses of OLE, propolis, and dimethyl sulfoxide, propolis diluent, for Hep-2 (ATCC, CCL-23) cells were determined by conventional cell culture. Using"endpoint"method, the viral dose infecting half of the cell culture (TCID50) was calculated, and viral quantity was determined with Spearman-Karber method. Antiviral effects of OLE and propolis on HSV-1 were investigated by conventional cell culture and real-time cell analysis (RTCA). Combinations of the two extracts with one another and with acyclovir were evaluated by RTCA. Active substances prepared at three different dilutions were added to tubes with HSV-1 of logTCID50: 11.5 in descending order starting from the highest non-toxic concentration, and they were left at room temperature for two different durations (one hour and three hours). The aliquots taken from the tubes were cultured in plates containing Hep-2 cells and evaluated after 72 hours. Combinations of extracts and acyclovir at concentrations at least four times lower than the lowest concentration showing antiviral efficacy against HSV-1 were cultured with Hep-2 cells in the e-plates of the xCELLigence RTCA device, measurements were obtained at 30 minute intervals, and data were recorded in real time. In the test with two different durations and at different concentrations of OLE and propolis, antiviral efficacy was observed both with one-hour and three-hour incubation at a concentration of 10μg/ ml for propolis and 1.2 mg/ml for OLE with RTCA. The duration and concentration of the greatest decrease in viral quantity were in the first one hour and 10 μg/ml for propolis, and in the first one hour and 1.2 mg/ ml for OLE. Combination of propolis and OLE with acyclovir caused no cytopathiceffects, and the combination of extracts led to delayed cytopathic effect. According to these results, propolis and OLE, alone and in combinations with acyclovir, have antiviral efficacy against HSV-1. These agents may reduce the dose and side effects of acyclovir in case of co-administration sincethey exert their effects through a different mechanism than acyclovir,possibly through direct virucidal activity, inhibition of virus internalization or viral inhibition in early stages of replication (inhibition of adsorption/binding of viral particles to the cell). These extracts that do not require conversion to active form have the potential to reduce infectivity in oral lesions, prevent spread, and be used in the topical treatment of acyclovir-resistant HSV infections, particularly in immunocompromised patients. However, in vivo studies should be conducted to determine their medicinal properties and potential toxicities. These results should be supported by further comprehensive studies and the efficacy against other viruses should also be investigated.


greenmedinfo--2020-03-30--Cytotoxic and apoptotic effects of ethanolic propolis extract on C6 glioma cells.

Propolis is a natural resinous substance obtained from beehives , and emerging evidence supports that it has antitumor , antiinflammatory @ @ @ @ @ activities .
The aim of the study is to examine the cytotoxic , antioxidant , @ @ @ @ @ propolis extract ( PE ) on C6 glioma cells .
The cells were treated with @ @ @ @ @ for 24 hours , after which the total antioxidant status ( TAS ) and total @ @ @ @ @ protein carbonyl , 8-hydroxy-2'-deoxyguanosine , and glutathione ( GSH ) levels ; Cu/Zn-superoxide dismutase ( @ @ @ @ @ apoptotic markers were measured .
Ethanolic PE at 100 , 250 , and 500 μg/mL @ @ @ @ @ C6 glioma cells .
TAS and GSH levels were significantly increased in C6 glioma cells @ @ @ @ @ μg/mL PE compared to control cells ( P

Propolis is a natural resinous substance obtained from beehives, and emerging evidence supports that it has antitumor, antiinflammatory, antioxidant, and antimicrobial activities. The aim of the study is to examine the cytotoxic, antioxidant, and apoptotic features of ethanolic propolis extract (PE) on C6 glioma cells. The cells were treated with ethanolic PE at various concentrations for 24 hours, after which the total antioxidant status (TAS) and total oxidant status; malondialdehyde, protein carbonyl, 8-hydroxy-2'-deoxyguanosine, and glutathione (GSH) levels; Cu/Zn-superoxide dismutase (Cu/Zn-SOD) activity; and apoptotic markers were measured. Ethanolic PE at 100, 250, and 500 μg/mL concentrations showed optimal activity on C6 glioma cells. TAS and GSH levels were significantly increased in C6 glioma cells treated with 100 and 500 μg/mL PE compared to control cells (P < .05). Similarly, the activity of Cu/Zn-SOD was higher in C6 glioma cells treated with 250 or 500 μg/mL ethanolic PE compared to control cells (P < .05), as was the caspase-3 mRNA expression level. The highest levels of caspase-8 and -9 expression were in C6 glioma cells treated with 500 μg/mL PE. Collectively, our results indicate that ethanolic PE has cytotoxic and apoptotic effects on C6 glioma cells. Furthermore, it may provide a protective role in the antioxidant defense system. PE shows potential for development as a natural antioxidant and apoptotic agent for the treatment of brain tumors.


greenmedinfo--2020-03-30--Effect of topical administration of propolis in chronic periodontitis.

To investigate the effect of topical administration of propolis ( a honeybee product ) or curry leaf ( an herbal product ) into the periodontal pockets of periodontitis patients , a double-blind controlled clinical trial was conducted with 24 subjects including one drop-out diagnosed with moderate-to-advanced chronic periodontitis who completed initial periodontal therapy .
They were randomly allocated to the following treatments : placebo , propolis , curry leaf , and minocycline .
Gingival crevicular fluid ( GCF ) samples collected before and after the intervention were analyzed to quantify the number of total bacteria and number of six major @ @ @ @ @ @ @ clinical parameters were also analyzed .
Among the six propolis-treated patients whose GCF samples were P. gingivalis-positive , three patients converted to be P. gingivalis-negative after the intervention .
The minocycline-treated group exhibited a decrease in probing pocket depth ( PPD ) with statistically significant improvement , but not gain of clinical attachment level ( CAL ) .
Both PPD and CAL have been improved in the propolis-treated group at a statistically significant level , but not the curry leaf-treated group .
In conclusion , treatment with propolis significantly improved both PPD and @ @ @ @ @ @ @ reduced P. gingivalis burden in GCF .
It is likely that a propolis-based therapy becomes an alternative treatment option for chronic periodontitis during supportive periodontal therapy .

To investigate the effect of topical administration of propolis (a honeybee product) or curry leaf (an herbal product) into the periodontal pockets of periodontitis patients, a double-blind controlled clinical trial was conducted with 24 subjects including one drop-out diagnosed with moderate-to-advanced chronic periodontitis who completed initial periodontal therapy. They were randomly allocated to the following treatments: placebo, propolis, curry leaf, and minocycline. Gingival crevicular fluid (GCF) samples collected before and after the intervention were analyzed to quantify the number of total bacteria and number of six major periodontopathic bacteria by real-time PCR. Periodontitis-related clinical parameters were also analyzed. Among the six propolis-treated patients whose GCF samples were P. gingivalis-positive, three patients converted to be P. gingivalis-negative after the intervention. The minocycline-treated group exhibited a decrease in probing pocket depth (PPD) with statistically significant improvement, but not gain of clinical attachment level (CAL). Both PPD and CAL have been improved in the propolis-treated group at a statistically significant level, but not the curry leaf-treated group. In conclusion, treatment with propolis significantly improved both PPD and CAL, together with a tendency towards reduced P. gingivalis burden in GCF. It is likely that a propolis-based therapy becomes an alternative treatment option for chronic periodontitis during supportive periodontal therapy.


greenmedinfo--2020-03-30--Propolis exhibited strong antihyperglycemic, antihyperlipidemic, and hepato-renal protective effects

Propolis exhibited strong antihyperglycemic, antihyperlipidemic, and hepato-renal protective effects in diabetes.

Objectives : The effect of propolis collected in Morocco on blood glucose , lipid profile , liver enzymes , and kidney function was investigated in control and diabetic rats .
Materials and Methods : Antioxidant activity of propolis was evaluated with the use of DPPH , 2,2'-azino-bis ( 3-ethylbenzothiazoline-6-sulphonic acid ) ( ABTS•+ ) , ferric reducing power and total antioxidant activity assay .
To study its effect in streptozotocin ( STZ ) -induced diabetes , the rats were divided into eight groups ; four control and four diabetics .
The animals received distilled water , glibenclamide , or propolis @ @ @ @ @ @ @ mg/kg/b.wt , daily for 15 days .
Blood glucose , triglyceride , lactic acid dehydrogenase , liver enzymes , creatinine , blood urea , lipid profile , and body weight were measured on day 15 after commencement of the treatment .
Results : Propolis has a strong antioxidant activity and high total flavonoids and polyphenols content .
Glibenclamide and propolis have no significant effect on lipid parameters , and renal and hepatic function in non-diabetic rats .
However , propolis or glibenclamide caused a significant lowering of blood glucose after a single administration @ @ @ @ @ @ @ in diabetic rats ( < 0.05 ) .
Both interventions significantly lowered lactic acid dehydrogenase , increased body weight , and ameliorated dyslipidemia and abnormal liver and kidney function caused by diabetes .
The effect of propolis was dose-dependent and in a high dose it was more potent than glibenclamide .
Conclusion : Propolis exhibited strong antihyperglycemic , antihyperlipidemic , and hepato-renal protective effects in diabetes , and significantly lowered the elevated lactic acid dehydrogenase .
The study demonstrated for the first-time the effect of Moroccan propolis in diabetes and it will pave @ @ @ @ @ @

Objectives: The effect of propolis collected in Morocco on blood glucose, lipid profile, liver enzymes, and kidney function was investigated in control and diabetic rats.
Materials and Methods: Antioxidant activity of propolis was evaluated with the use of DPPH, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS•+), ferric reducing power and total antioxidant activity assay. To study its effect in streptozotocin (STZ)-induced diabetes, the rats were divided into eight groups; four control and four diabetics. The animals received distilled water, glibenclamide, or propolis extract, 50 mg/kg/BW) or 100 mg/kg/b.wt, daily for 15 days. Blood glucose, triglyceride, lactic acid dehydrogenase, liver enzymes, creatinine, blood urea, lipid profile, and body weight were measured on day 15 after commencement of the treatment.
Results: Propolis has a strong antioxidant activity and high total flavonoids and polyphenols content. Glibenclamide and propolis have no significant effect on lipid parameters, and renal and hepatic function in non-diabetic rats. However, propolis or glibenclamide caused a significant lowering of blood glucose after a single administration and at day 15 after daily administration in diabetic rats (<0.05). Both interventions significantly lowered lactic acid dehydrogenase, increased body weight, and ameliorated dyslipidemia and abnormal liver and kidney function caused by diabetes. The effect of propolis was dose-dependent and in a high dose it was more potent than glibenclamide.
Conclusion: Propolis exhibited strong antihyperglycemic, antihyperlipidemic, and hepato-renal protective effects in diabetes, and significantly lowered the elevated lactic acid dehydrogenase. The study demonstrated for the first-time the effect of Moroccan propolis in diabetes and it will pave the way for clinical investigations.


greenmedinfo--2020-03-30--The Cuban propolis component nemorosone inhibits proliferation and metastatic properties of human co

The Cuban propolis component nemorosone inhibits proliferation and metastatic properties of human colorectal cancer cells.

The majority of deaths related to colorectal cancer ( CRC ) are associated with the metastatic process .
Alternative therapeutic strategies , such as traditional folk remedies , deserve attention for their potential ability to attenuate the invasiveness of CRC cells .
The aim of this study is to investigate the biological activity of brown Cuban propolis ( CP ) and its main component nemorosone ( NEM ) and to describe the molecular mechanism ( s ) by which they inhibit proliferation and metastatic potential of 2 CRC cell lines , i.e.
, HT-29 and LoVo .
Our results show @ @ @ @ @ @ @ viability and inhibited clonogenic capacity of CRC cells in a dose and time-dependent manner , by arresting the cell cycle in the G0/G1 phase and inducing apoptosis .
Furthermore , CP and NEM downregulatedgene expression and upregulated the expression of the proapoptotic genesand , with a consequent activation of caspase 3/7 .
They also attenuated cell migration and invasion by inhibiting MMP9 activity , increasing E-cadherin and decreasingβ-catenin and vimentin expression , proteins involved in the epithelial-mesenchymal transition ( EMT ) .
In conclusion NEM , besides displaying antiproliferative activity on CRC cells @ @ @ @ @ @ @ potential by modulating EMT-related molecules .
These finding provide new insight about the mechanism ( s ) of the antitumoral properties of CP , due to NEM content .

The majority of deaths related to colorectal cancer (CRC) are associated with the metastatic process. Alternative therapeutic strategies, such as traditional folk remedies, deserve attention for their potential ability to attenuate the invasiveness of CRC cells. The aim of this study is to investigate the biological activity of brown Cuban propolis (CP) and its main component nemorosone (NEM) and to describe the molecular mechanism(s) by which they inhibit proliferation and metastatic potential of 2 CRC cell lines, i.e., HT-29 and LoVo. Our results show that CP and NEM significantly decreased cell viability and inhibited clonogenic capacity of CRC cells in a dose and time-dependent manner, by arresting the cell cycle in the G0/G1 phase and inducing apoptosis. Furthermore, CP and NEM downregulatedgene expression and upregulated the expression of the proapoptotic genesand, with a consequent activation of caspase 3/7. They also attenuated cell migration and invasion by inhibiting MMP9 activity, increasing E-cadherin and decreasingβ-catenin and vimentin expression, proteins involved in the epithelial-mesenchymal transition (EMT). In conclusion NEM, besides displaying antiproliferative activity on CRC cells, is able to decrease their metastatic potential by modulating EMT-related molecules. These finding provide new insight about the mechanism(s) of the antitumoral properties of CP, due to NEM content.


greenmedinfo--2020-03-30--Ethanol extract of propolis prevents high-fat diet-induced insulin resistance and obesity in associa

Ethanol extract of propolis prevents high-fat diet-induced insulin resistance and obesity in association with modulation of gut microbiota.

Propolis has beneficial effects anti-inflammatory , anti-diabetes and anti-obesity in human or murine models , but its mechanism has not been fully elucidated .
This study was to investigate the effects of ethanol extract of propolis ( EEP ) on the gut microbiota , and to analyze the associations between these alterations of gut microbiota and insulin resistance and obesity in high fat diet ( HFD ) -fed mice .
Male C57BL/6J mice were fed with chow diet , high-fat diet , and high-fat diet supplemented with 1 % EEP or 2 % EEP .
EEP supplementation reduced HFD-induced weight @ @ @ @ @ @ @ cytokines and insulin resistance , and improved glucose tolerance and lipid profile .
Meanwhile , EEP supplementation in HFD-fed mice increased anti-obesity and anti-inflammatory bacteria such as genera Roseburia and Intestinimonas and species Parabacteroides goldsteinii and Parabacteroides distasonis , and reduced pro-inflammatory bacteria such as genera Faecalibaculum and Prevotella and species Bacteroides vulgatus .
These dominant bacterial taxa altered by EEP were significantly associated with the metabolic parameters of insulin resistance and obesityin HFD-fed mice .
The results in this study indicated that EEP reduced HFD-induced obesity and insulin resistant , which may @ @ @ @ @ @ @ function of gut microbiota .

Propolis has beneficial effects anti-inflammatory, anti-diabetes and anti-obesity in human or murine models, but its mechanism has not been fully elucidated. This study was to investigate the effects of ethanol extract of propolis (EEP) on the gut microbiota, and to analyze the associations between these alterations of gut microbiota and insulin resistance and obesity in high fat diet (HFD)-fed mice. Male C57BL/6J mice were fed with chow diet, high-fat diet, and high-fat diet supplemented with 1% EEP or 2%EEP. EEP supplementation reduced HFD-induced weight gain and liver fat accumulation, proinflammatory cytokines and insulin resistance, and improved glucose tolerance and lipid profile. Meanwhile, EEP supplementation in HFD-fed mice increased anti-obesity and anti-inflammatory bacteria such as genera Roseburia and Intestinimonas and species Parabacteroides goldsteinii and Parabacteroides distasonis, and reduced pro-inflammatory bacteria such as genera Faecalibaculum and Prevotella and species Bacteroides vulgatus. These dominant bacterial taxa altered by EEP were significantly associated with the metabolic parameters of insulin resistance and obesityin HFD-fed mice. The results in this study indicated that EEP reduced HFD-induced obesity and insulin resistant, which may be mediated by modulating the composition and function of gut microbiota.


greenmedinfo--2020-03-30--Quercetin suppresses migration and invasion by targeting miR-146a/GATA6 axis in fibroblast-like syno

Quercetin suppresses migration and invasion by targeting miR-146a/GATA6 axis in fibroblast-like synoviocytes of rheumatoid arthritis.

Rheumatoid arthritis ( RA ) is a systematic autoimmune disease which may lead to joint dysfunction and disability .
Aberrant migration and invasion of fibroblast-like synoviocytes ( FLSs ) is one of the most predominant etiopathogenesis of RA .
Quercetin is a bioflavonoid which is implicated in the development of RA , yet its role in regulating the migration and invasion of FLSs is still elusive .
The aim of this study is to investigate the impact of quercetin treatment on migration and invasion of FLSs and the underlying mechanism.Capacity of migration and invasion of FLSs were assessed using transwell @ @ @ @ @ @ @ determine the expression of F-actin .
The RNA levels of miR-146a and GATA transcription factor 6 ( GATA6 ) were measured using quantitative real-time PCR .
Western blot was used to examine the protein level of GATA6 .
The correlation between miR-146a and GATA6 was validated using luciferase reporter assay.Transwell assay revealed that the migration and invasion of FLSs were significantly inhibited after quercetin treatment , which was also proved by decreased expression of F-actin .
The RNA level of miR-146a was decreased in RA tissues and was negatively related to the expression @ @ @ @ @ @ @ ) .
Quercetin treatment elevated the RNA level of miR-146a , but suppressed the expression of GATA6 in FLSs .
Further luciferase reporter assay validated that GATA6 is a downstream target of miR-146a .
Besides , miR-146a inhibited the migration and invasion of FLSs , and further GATA6 over-expression abrogated the miR-146a-induced inhibition .
In addition , specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis .

Rheumatoid arthritis (RA) is a systematic autoimmune disease which may lead to joint dysfunction and disability. Aberrant migration and invasion of fibroblast-like synoviocytes (FLSs) is one of the most predominant etiopathogenesis of RA. Quercetin is a bioflavonoid which is implicated in the development of RA, yet its role in regulating the migration and invasion of FLSs is still elusive. The aim of this study is to investigate the impact of quercetin treatment on migration and invasion of FLSs and the underlying mechanism.Capacity of migration and invasion of FLSs were assessed using transwell assay. Immunofluorescence assay was used to determine the expression of F-actin. The RNA levels of miR-146a and GATA transcription factor 6 (GATA6) were measured using quantitative real-time PCR. Western blot was used to examine the protein level of GATA6. The correlation between miR-146a and GATA6 was validated using luciferase reporter assay.Transwell assay revealed that the migration and invasion of FLSs were significantly inhibited after quercetin treatment, which was also proved by decreased expression of F-actin. The RNA level of miR-146a was decreased in RA tissues and was negatively related to the expression of GATA transcription factor 6 (GATA6). Quercetin treatment elevated the RNA level of miR-146a, but suppressed the expression of GATA6 in FLSs. Further luciferase reporter assay validated that GATA6 is a downstream target of miR-146a. Besides, miR-146a inhibited the migration and invasion of FLSs, and further GATA6 over-expression abrogated the miR-146a-induced inhibition. In addition, specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis.