Mangiferin ameliorates placental oxidative stress and activates PI3K/Akt/mTOR pathway in mouse model of preeclampsia
Archives of Pharmacal Research(2020)
摘要
Preeclampsia is an inflammatory disease which can induce oxidative stress in placenta. Oxidative stress in 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 and brain through activating the PI3K/Akt/mTOR pathway. We aimed to investigate the effects of mangiferin in a mouse model of preeclampsia, which was induced by phosphatidylserine/dioleoyl-phosphatidycholine (PS/PC) from day 5 to 17 of pregnancy. The female pregnant mice were divided into five groups according to drug treatment. Animals received mangiferin orally at doses of 10, 20, 40 mg/kg/day from day 0.5 to 17. In preeclampsia mouse model, elevated systolic blood pressure and proteinuria were ameliorated by mangiferin treatment. Mangiferin attenuated fms-like tyrosine kinase-1 and placental growth factor expression and oxidative stress in both blood and placenta of preeclampsia mice. The suppressed PI3K/Akt/mTOR pathway in placenta was activated by mangiferin treatment. This study demonstrates that mangiferin ameliorates placental oxidative stress and activates PI3K/Akt/mTOR pathway in a mouse model of preeclampsia.
更多查看译文
关键词
Preeclampsia, Phosphatidylinositol-3-Kinase/Akt/Mammalian Target of Rapamycin pathway, Mangiferin
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要