Fisetin对H9C2细胞中IGF-IR-PI3K-AKT信号的激活和自发性高血压大鼠的激活对血管紧张素II诱导的细胞凋亡的保护作用。
摘要来源：摘要来源：
phytomedicine。 2019年4月； 57：1-8。 EPUB 2018年9月17日。PMID： 306668312 30668312 Marthandam Asokan Shibu，Rajendran Peramaiyan，Cecilia hsuan Day，Chia-Yao Shen，Chao-Hung Lai，Ray-Jade Chen，Vijaya Padma Viswanadha，Ya-fang chen，Ya-fang chen，Chih-Yang Huang Huang Huang
ye ye p> ye p> yh p> class =“ sub_abstract_label”>背景： fisetin，一种多酚化合物，由于其抗氧化剂，抗炎，抗癌和神经保护作用，引起了人们的关注。但是，fisetin的心脏影响尚不清楚。假设： aim of the present study is to examine the cardioprotective effect of fisetin against Ang-II induced apoptosis in H9c2 cells and in spontaneous hypertensive rats (SHR).
METHODS/STUDY DESIGN: The in vitro protective effect of fisetin was evaluated after the cells were treated with fisetin （50 µm/ ml/ 24 h）在ANG-II给药前2小时诱导凋亡。对于体内实验，SHR SHR每周两次用Fisetin（10 mg/kg）口服6周。 Cellular apoptosis was analyzed by TUNEL staining assay and the modulation in the expression levels of proteins involved in apoptosis and cell survival were determined by western blotting.
RESULTS: Our results demonstrate the potent cardioprotective efficacy of fisetin against Ang-II induced apoptosis in H9C2细胞和SHR模型。 fisetin给药可大大降低凋亡核nd reduced the expression of apoptotic proteins such as TNF-α, Fas L, FADD, Cleaved caspase-3 and Cleaved PARP and increased the cell survival and anti-apoptotic proteins like Bcl-2, Bcl-xp-IGF1R, p-PI3K and p-AKT in both in vitro and in vivo models.
结论： 总而言之，本研究的结果表明，fisetin激活IGF-IR依赖性P-PI3K/P-AKT存活信号传导途径并抑制Caspase依赖性凋亡。