We evaluated the effects of administration of 1,25-dihydroxyvitamin D 
(1,25(OH)2D) during pregnancy on relieving adverse outcomes of preeclampsia and 
the pathologic and biochemical changes in reduction in uteroplacental perfusion 
(RUPP) model of rats. On day 1, 7, and 14 of pregnancy, rats in pregnant RUPP 
plus 1,25(OH)2D (RUPP+VD) group (n = 15) received 120 ng/100 g body weight/week 
of 1,25(OH)2D by subcutaneous injection, while rats in normal pregnant (n = 12) 
and the RUPP group (n = 14) received 1,25(OH)2D vehicle (saline solution). On 
day 19 of pregnancy, after measure of blood pressure and cardiac function and 
urine collection, rats were euthanized, and fetal and maternal serum, placenta, 
and heart and kidney were collected. Fetal mortality, urinary protein, glucose, 
and parameters for kidney function in serum were measured. We evaluated vitamin 
D receptor expression and pathological and ultrastructural changes in rat heart, 
kidney, and placenta. Levels of oxidative stress, endoplasmic reticulum (ER) 
stress, apoptosis, and autophagy were measured in placenta. Compared to RUPP 
rats, 1,25(OH)2D decreased fetal mortality, mean blood pressure, 24-h urinary 
protein, urine microalbumin, and hyperglycemia in RUPP+VD rats. These were 
consistent with the improvements of structure impairment in heart, kidney, and 
placenta of RUPP rat by 1,25(OH)2D. In placenta of RUPP rat, the decrease in 
oxidative stress and ER stress by 1,25(OH)2D treatment was accompanied by 
autophagy activation and apoptosis attenuation. 1,25(OH)2D plays a beneficial 
effect on preeclampsia at the early gestation and might be used as a potential 
protective agent for preeclampsia. However, the RUPP model only recapitulated 
the hypoxic origin of preeclampsia; further randomized controlled trial is 
expected to be performed for validation and evaluation.