251. Isorhamnetin: A hepatoprotective flavonoid inhibits apoptosis and autophagy via P38/PPAR-α pathway in mice
- Author
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Xiya Lu, Xiaoming Fan, Chuanyong Guo, Sainan Li, Yingqun Zhou, Jiao Feng, Liwei Wu, Kan Chen, Peiqin Niu, Yujing Xia, Fan Wang, Shizan Xu, Tong Liu, Weiqi Dai, Jingjing Li, Ling Xu, Qiang Yu, and Wenwen Wang
- Subjects
0301 basic medicine ,Male ,MAP Kinase Signaling System ,p38 mitogen-activated protein kinases ,Peroxisome proliferator-activated receptor ,Apoptosis ,Pharmacology ,Proinflammatory cytokine ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,Autophagy ,Concanavalin A ,Animals ,PPAR alpha ,Isorhamnetin ,chemistry.chemical_classification ,Mice, Inbred BALB C ,biology ,General Medicine ,030104 developmental biology ,chemistry ,biology.protein ,Quercetin ,Chemical and Drug Induced Liver Injury ,Inflammation Mediators - Abstract
Isorhamnetin, a flavonoid compound extracted from plants' fruit or leaves, like sea buckthorn (Hippophae rhamnoides L.), has many biological functions, including anti-tumor, anti-oxidant and anti-inflammatory effect. The present study is in order to explore the hepatoprotective effect of isorhamnetin on concanavalin A (ConA)-induced acute fulminant hepatitis and the underlying mechanism. Mice were injected with ConA (25 mg/kg) to induce acute fulminant hepatitis, three doses of isorhamnetin (10/30/90 mg/kg) was intraperitoneally administrated about 1 h previously. The serum and liver tissues were harvested at 2, 8, and 24 h after ConA injection. The levels of serum liver enzymes and proinflammatory cytokines were significantly reduced in isorhamnetin administration groups. Besides, isorhamnetin improved pathological damage. Furthermore, isorhamnetin affected P38/PPAR-α pathway, and subsequently regulated the expression of apoptosis and autophagy related proteins. The present study investigated that isorhamnetin inhibits apoptosis and autophagy via P38/PPAR-α pathway in mice.
- Published
- 2017