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Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-355556

RESUMO

<p><b>OBJECTIVE</b>To investigate the effects of curcumin on the apoptosis of ischemia/reperfusion (I/R) induced H9c2 myocardial cells and the expression of glycogen synthase kinase-3 (GSK-3) and its phosphorylation state.</p><p><b>METHODS</b>I/R of H9c2 cells in vitro was simulated by an ischemic Tyrode solution. Cells were randomly divided into 3 groups, i.e., the model group (exposed to ischemic solution for 90 min followed by 30 min reperfusion with the normal Tyrode solution), the curcumin group (7.5 micromol/L curcumin added at the onset of reperfusion for 30 min), and the control group (exposed to normal Tyrode solution for 120 min). Then, the cell apoptosis was detected in 3 groups by flow cytometry. The expression levels of GSK-3, phosphotyrosine-GSK-3 (pTyr-GSK-3), and phosphoserine-GSK-3 (pSer-GSK-3) were detected by Western blot.</p><p><b>RESULTS</b>Compared with the control group,the apoptosis rate was obviously enhanced in the model group (t = 10.439, P = 0.000). And the relative expression levels of both pTyr-GSK-3 and pSer-GSK-3 significantly increased in the model group (t = 5.208, P = 0.006; t = 5.854, P = 0.004, respectively). Compared with the model group, the apoptosis rate and the expression of pTyr-GSK-3 significantly decreased in the curcumin group (t = -8.325, P = 0.001; t = -3.607, P = 0.023). Compared with the model group, the rate of viable cells and the expression of pSer-GSK-3 were significantly enhanced in the curcumin group (t = 9.165, P = 0.001; t = 3.747, P = 0.02).</p><p><b>CONCLUSIONS</b>Both pTyr-GSK-3 and pSer-GSK-3 might participate in the IR injured myocardial cells. Curcumin could reduce apoptosis of I/R injured myocardial cells, which might be correlated with GSK-3 inhibition by decreasing tyrosine phosphorylation and increasing serine phosphorylation.</p>


Assuntos
Animais , Ratos , Apoptose , Linhagem Celular , Curcumina , Farmacologia , Quinase 3 da Glicogênio Sintase , Metabolismo , Traumatismo por Reperfusão Miocárdica , Metabolismo , Miócitos Cardíacos , Metabolismo , Fosforilação , Traumatismo por Reperfusão , Patologia , Transdução de Sinais
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