Ischemic preconditioning Smad 3 protein expression by inhibiting the reduction of cardiomyocyte apoptosis in experimental study.docVIP
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Ischemic preconditioning Smad 3 protein expression by inhibiting the reduction of cardiomyocyte apoptosis in experimental study
PAGE \* MERGEFORMAT 13
Ischemic preconditioning Smad 3 protein expression by inhibiting the reduction of cardiomyocyte apoptosis in experimental study
Authors: Xiao Jian, Zhi-Nong Wang, Zhu Zhen, Sheng-Dong Huang, Zhi-Yun Xu, Bao-Ren Zhang
[Abstract] Objective To investigate the Smad 3 protein (small mother against decapentaplegic) in myocardial ischemia-reperfusion injury and myocardial apoptosis in relationships. Methods neonatal SD rat cardiomyocytes were randomly divided into three groups: ① normal control group (A group): In the non-treatment factors, with 10% FBS DMEM culture medium in the aerobic incubator (37 ℃ , 5% CO2 and 95% air) in cultured 48 h; ② ischemia-reperfusion (IR)-induced apoptosis in model group (B group): serum-free DMEM culture medium in the hypoxia incubator sugar (95% N2 and 5% CO2) in the After 48 h culture, and then 10% FBS DMEM culture medium in the aerobic incubator 3 h; ③ ischemic preconditioning (IPC) group (C group): serum-free DMEM culture medium in the hypoxia sugar incubator, after 6 h, and then 10% FBS DMEM culture medium in the aerobic incubator 3 h, further ischemia-reperfusion (step with the B group). Results A group, B group and C group of cardiac myocyte apoptosis rates were (5.89 ± 1.28)%, (26.68 ± 6.17)%, (12.45 ± 1.52)%, with a significant statistical difference. Three groups of cells, the expression of Smad 3 were (21.77 ± 2.32)%, (35.7 ± 2.43)%, (29.47 ± 1.36)%, with a significant statistical difference. Conclusion Smad 3 can induce myocardial ischemia-reperfusion injury in myocardial apoptosis and ischemic preconditioning could inhibit the expression of Smad 3, thereby protecting myocardial cells.
[Keywords:] ischemia-reperfusion; ischemic preconditioning; Smad 3; myocardial cells; apoptosis
Abstract: OBJECTIVE To research the relationship of Smad 3 and myocardiocyte apoptosis stimulated by ischemia reperfusion injury (IR). METHODS The myocardiocytes of neonatal SD rats were divided randomly into 3
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