부산대학교 도서관

Preeclampsia is an inflammatory disease whichcan induce oxidative stress in placenta. Oxidative stressin preeclampsia is regulated by the phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway. Mangiferin, an anti-oxidative molecule,is reported to ameliorate oxidative stress in the kidney andbrain through activating the PI3K/Akt/mTOR pathway. Weaimed to investigate the effects of mangiferin in a mousemodel of preeclampsia, which was induced by phosphatidylserine/dioleoyl-phosphatidycholine (PS/PC) from day 5to 17 of pregnancy. The female pregnant mice were dividedinto five groups according to drug treatment. Animalsreceived mangiferin orally at doses of 10, 20, 40 mg/kg/dayfrom day 0.5 to 17. In preeclampsia mouse model, elevatedsystolic blood pressure and proteinuria were ameliorated bymangiferin treatment. Mangiferin attenuated fms-like tyrosinekinase-1 and placental growth factor expression andoxidative stress in both blood and placenta of preeclampsiamice. The suppressed PI3K/Akt/mTOR pathway in placentawas activated by mangiferin treatment. This study demonstratesthat mangiferin ameliorates placental oxidative stressand activates PI3K/Akt/mTOR pathway in a mouse modelof preeclampsia.