细胞凋亡
缺氧(环境)
化学
染料木素
下调和上调
分子生物学
活力测定
免疫印迹
半胱氨酸蛋白酶3
程序性细胞死亡
药理学
生物
内分泌学
生物化学
基因
有机化学
氧气
作者
Yaning Shi,Xiuqin Zhang,Zheyu Hu,Chanjuan Zhang,Duan‐Fang Liao,Honglin Huang,Qin Li
出处
期刊:Pharmacology
[S. Karger AG]
日期:2019-01-01
卷期号:103 (5-6): 282-290
被引量:28
摘要
<b><i>Background/Aims:</i></b> Hypoxia can induce cell injury in cardiomyocytes and further lead to cardiovascular diseases. Genistein (Gen), the predominant isoflavone found in soy products, has shown protective effects on cardiovascular system. The aim of the present study was to investigate the cardioprotective effect of Gen against chemical hypoxia-induced injury. <b><i>Methods:</i></b> Cobalt chloride (CoCl<sub>2</sub>) was administrated to trigger chemical hypoxia in H9c2 cardiomyocytes. Cell proliferation was detected by using MTT assay. The expression level of hypoxia-related proteins (hypoxia-inducible factor [HIF]-1α and Notch-1) and apoptosis-related proteins (B cell lymphoma [Bcl]-2, Bax, and caspase-3) were evaluated by Western blot analysis. <b><i>Results:</i></b> In response to hypoxia, cell viability was reduced dramatically, whereas the expression of HIF-1α was upregulated. Hypoxia also induced cardiomyocytes apoptosis by reducing the ratio of Bcl-2/Bax and increasing expression of caspase-3. Interestingly, Gen attenuated CoCl<sub>2</sub>-induced cell death and suppressed HIF-1α expression, as well as upregulated the expression of Notch-1. Furthermore, Gen could antagonize CoCl<sub>2</sub>-induced apoptosis through upregulating Bcl-2/Bax ratio and inhibiting caspase-3 expression. <b><i>Conclusions:</i></b> Gen prevents chemical hypoxia-induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, exerting protective effects on H9c2 cardiomyocytes.
科研通智能强力驱动
Strongly Powered by AbleSci AI