Key result
Genistein attenuates CoCl2-induced cardiomyocyte death by upregulating the Bcl-2/Bax ratio and inhibiting caspase-3.
Why the study?
Hypoxia induces cardiomyocyte injury leading to cardiovascular diseases, and the cardioprotective effects of genistein against chemical hypoxia-induced injury require investigation.
Does Genistein protect H9c2 cardiomyocytes against chemical hypoxia-induced injury?
Does Genistein protect H9c2 cardiomyocytes against chemical hypoxia-induced injury?
Genistein protects H9c2 cardiomyocytes against chemical hypoxia-induced apoptosis by inhibiting the mitochondrial apoptotic pathway.
Answers are grounded in this paper and cite their sources.
Should not yet inform clinical practice in hypoxic injury; leaves open further exploration of mitochondrial apoptosis modulation in cardiomyocytes.
BACKGROUND/AIMS: 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. METHODS: Cobalt chloride (CoCl2) 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. RESULTS: 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 CoCl2-induced cell death and suppressed HIF-1α expression, as well as upregulated the expression of Notch-1. Furthermore, Gen could antagonize CoCl2-induced apoptosis through upregulating Bcl-2/Bax ratio and inhibiting caspase-3 expression. CONCLUSIONS: Gen prevents chemical hypoxia-induced cell apoptosis through inhibition of the mitochondrial apoptotic pathway, exerting protective effects on H9c2 cardiomyocytes.
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Shi et al. (2019) studied Chemical hypoxia-induced injury. Genistein vs. Cobalt chloride (CoCl2) alone was evaluated on Cell viability and apoptosis. Genistein attenuated CoCl2-induced cell death and apoptosis in H9c2 cardiomyocytes by upregulating the Bcl-2/Bax ratio and inhibiting caspase-3 expression.
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