自噬
PI3K/AKT/mTOR通路
蛋白激酶B
MAPK/ERK通路
心脏毒性
下调和上调
吖啶橙
心肌保护
化学
木犀草素
药理学
程序性细胞死亡
饥饿
细胞生物学
激酶
生物化学
生物
信号转导
类黄酮
医学
内分泌学
内科学
细胞凋亡
毒性
抗氧化剂
有机化学
基因
缺血
作者
Hong Yao,Lichun Zhou,Linlin Tang,Yanhui Guan,Chao Shang,Yu Zhang,Xiuzhen Han
出处
期刊:BioScience Trends
[International Research and Cooperation Association for Bio & Socio-Sciences Advancement]
日期:2017-01-01
卷期号:11 (5): 557-564
被引量:16
标识
DOI:10.5582/bst.2017.01111
摘要
Cardiomyocyte nutrient deprivation is a common clinical event that mediates various cardiac ischemic processes and is associated with autophagy activation and cell survival or death. Luteolin-7-O-glucoside (LUTG) was one of the flavonoid glycosides isolated from Dracocephalum tanguticum. Previous research had showed that LUTG pretreatment had significant protective effects against doxorubicin-induced cardiotoxicity. However, whether LUTG could protect cardiomyocytes from starvation-induced injury was not clear. In this study, cardioprotection and mechanisms of LUTG against starvation-induced injury were investigated in vitro. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-tetrazolium bromide (MTT) assay showed starvation-induced autophagy is a homeostatic and protective response for H9c2 cell survival. LUTG could protect against injury induced by starvation in H9c2 cells. Acridine orange (AO) staining showed that pretreatment with LUTG enhanced lysosomal autophagy. Western blotting indicated that LUTG enhanced autophagy by down-regulating the expression of phospho-extracellular signal regulated kinase1/2 (p-ERK), phospho-protein kinase B (p-Akt) and phospho-mammalian target of rapamycin (p-mTOR). These results suggest that LUTG might act as a promising therapeutic agent for preventing starvation-induced cardiotoxicity by upregulation of autophagy through the Akt/mTOR and ERK signal pathway.
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