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  • Title: Heme oxygenase-1 ameliorates hypoxia/reoxygenation via suppressing apoptosis and enhancing autophagy and cell proliferation though Sirt3 signaling pathway in H9c2 cells.
    Author: Meng X, Yuan Y, Shen F, Li C.
    Journal: Naunyn Schmiedebergs Arch Pharmacol; 2019 Feb; 392(2):189-198. PubMed ID: 30415272.
    Abstract:
    Cardiomyocyte infarction could lead to high morbidity and mortality worldwide. Recent studies demonstrated that Heme oxygenase-1 (HO-1) could exert cardiac protective effect and arouse attention. However, the detailed mechanism is still unclear. Our study provided evidences of the protective effect of HO-1 overexpression on cardiomyocytes against hypoxia/reoxygenation (H/R). We divided the treatment into four groups: the control group, H/R group, H/R+HO-1 group, and H/R+Null group. Immunofluorescent study was utilized to label the BrdU-positive and LC3-positive cells. Flow cytometry and TUNEL assay were used to examine the cell apoptosis. Protein levels of Bax, Bcl-2, Sirt3, beclin-1, LC3-I, and LC3-II were both measured using western blotting. The results indicated that HO-1 overexpression decreased the cell apoptosis and enhanced the cell proliferation. The level of Sirt3 and autophagy were also increased in H/R+HO-1 group compared with H/R group. However, ZnPP, a HO-1 inhibitor, and SiRNA of Sirt3 are both reversed the decrease of cell apoptosis of HO-1 overexpression. Moreover, ZnPP also decreased the expression of Sirt3 in HO-1 overexpression treatment group. In summary, HO-1 overexpression protects cardiomyocytes against H/R injury via ameliorating cell apoptosis and enhancing cell proliferation and autophagy through Sirt3 signaling pathway.
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