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- W2392125412 abstract "Aim To investigate effects of trimetazidine on apoptosis and its signal regulation in human cardiomyocytes induced by hypoxia and reoxygenation. Methods Human cardiomyocytes were obtained from minced myocardium digested in trypsin and collagenase. The cultured cells apoptosis was induced by hypoxia and reoxygenation. Optional time of apoptosis was hypoxia 24 h and reoxygenation 4 h. The bcl-2, bax, caspase-3 and cytochrome C proteins were detected by using immunocytochemistry (ICC). Bcl-2 mRNA and caspase-3 mRNA were detected by using in situ hybridization method (ISH). Apoptosis signal was expressed by optical density. SPSS 10.0 was used for statistical analysis. Results (1). Twenty-four hours of hypoxia followed by 4 h of reoxygenation significantly increased the rate of apoptosis [(18.50±1.00)%]. Results revealed that H/R significantly induced the down-regulation of bcl-2 proteins(0.189±0.006)and up-regulation of bax(0.240±0.002), caspase-3(0.230±0.002)and cytochrome C(0.225±0.003)proteins;down-regulation of bcl-2 mRNA(0.300±0.003)and up-regulation of caspase-3 mRNA(0.307±0.004)in cardiomyocytes comparing with control group respectively (all P0.01). (2). Trimetazidine significantly decreased the rate of apoptotic, up-regulated the expression level of bcl-2 and down-regulated expression levels of bax, caspase-3 and cytochrome C protein, respectively (all P0.01). Trimetazidine also up-regulated the expression level of bcl-2 mRNA and down-regulated the expression level of caspase-3 mRNA. Conclusion Trimetazidine has anti-apoptosis effect and its mechanisms may be related to the increased expression levels of bcl-2 proteins and bcl-2 mRNA and decreased expression levels of bax, caspase-3, cytochrome C proteins and caspase-3 mRNA." @default.
- W2392125412 created "2016-06-24" @default.
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- W2392125412 date "2006-01-01" @default.
- W2392125412 modified "2023-09-25" @default.
- W2392125412 title "Effects of trimetazidine on apoptosis in human cardiomyocytes induced by hypoxia and reoxygenation" @default.
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