IGF-1 Protects Myocardial Cells from ROS Stress-Induced Apoptosis via Up-Regulating ARC

被引:0
作者
Xi, Zhaofang [1 ]
Zhu, Haibao [1 ]
Liu, Dongyang [1 ]
Wu, Liming [1 ]
Guo, DingZong [1 ]
机构
[1] Huazhong Agr Univ, Coll Vet Med, Wuhan 430070, Peoples R China
来源
JOURNAL OF ANIMAL AND VETERINARY ADVANCES | 2012年 / 11卷 / 11期
基金
高等学校博士学科点专项科研基金;
关键词
H9C2; cells; hydrogen peroxide; IGF-1; ARC; apoptosis; China; GROWTH-FACTOR-I; CASPASE RECRUITMENT DOMAIN; SKELETAL-MUSCLE; REPRESSOR; EXPRESSION; PATHWAY; REPERFUSION; ACTIVATION; INFARCTION; SURVIVAL;
D O I
暂无
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Insulin-like Growth Factor-1 (IGF-1) and Apoptosis Repressor with Caspase recruitment domain (ARC) play an important role in regulating apoptosis. Although, the precise mechanisms of IGF-1 and ARC in this process have not been defined, they have similar anti-apoptotic effects in myocardial cells, suggesting that these effects are related. Researchers found that H2O2 can induce ARC reduction in H9C2 cells but IGF-1 can change this trend. To clarify this trend using immunofluorescence and immunoblot analysis, researchers found that LY294002 (PI3K inhibitor) blocked IGF-1 up-regulation of ARC protein and blocked the protective effect of IGF-1 on myocardial cell apoptosis induced by oxidative stress. These results indicate that IGF-1 up-regulates ARC protein expression via the PI3K pathway which protects against myocardial cell apoptosis induced by oxidative stress.
引用
收藏
页码:1901 / 1906
页数:6
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