尼可地尔对波动性高糖诱导的大鼠心肌细胞H9C2凋亡的抑制作用

发布时间：2018-07-20 19:41

【摘要】：目的:探讨尼可地尔(Nicorandial)对波动性高糖诱导的大鼠心肌细胞(H9C2)凋亡的抑制作用,验证损伤与保护的可能的机制。方法:H9C2低糖培养基培养贴壁后进行分组,分别为A:低糖对照组;实验组B:波动性高糖组(B0:波动性高糖凋亡组;B1:波动性高糖+10μmol/L尼可尔保护组;B2:波动性高糖+50μmol/L尼可地尔保护组;B3:波动性高糖+100μmol/L尼可地尔保护组B);C:波动性高糖+100μmol/L尼可地尔+10μmol/L格列苯脲拮抗保护组。分别干预24小时后,应用CCK法检测各组细胞增殖情况;SOD活性、caspase-3活性验证细胞凋亡及保护;应用TUNEL法染色检测各组心肌细胞的凋亡形态以及计算凋亡率。结果:(1)与对照组相比,各实验组细胞增殖减少,凋亡现象严重,尼可地尔可抑制细胞的凋亡程度,且呈浓度依赖性;(2)与对照组相比,加不同浓度尼可地尔保护各组细胞CCK-8 OD450μm、SOD活性均降低,随浓度升高降低幅度减少,Caspase-3活性升高,随浓度上升增高幅度减少,TUNEL染色细胞凋亡增多,呈浓度依赖性;(3)波动性高糖+尼可地尔+格列苯脲心肌组CCK-8 OD450μm、SOD活性均降低较波动性凋亡组及低浓度尼可地尔保护组低,较中高浓度尼可地尔保护组高,Caspase-3活性及细胞凋亡率结果与SOD活性结果相反。结论:波动性高糖具有损伤心肌细胞的作用,可诱导其凋亡;尼可地尔具有心肌细胞保护的作用,且呈现浓度依赖性,其机制可能为K-ATP通道开放的作用。
[Abstract]:Aim: to investigate the inhibitory effect of Nicorandial on apoptosis of rat cardiomyocytes (H9C2) induced by volatile high glucose, and to verify the possible mechanism of injury and protection. Experimental group B: volatile high glucose group (B0: fluctuating high glucose apoptosis group B1: volatile high glucose 10 渭 mol / L Nicol protection group B2: volatile high sugar 50 渭 mol / L nicoradil protective group B3: volatile high glucose 100 渭 mol / L nicordil protective group B) C3: volatile high sugar 100 渭 mol / L Nicoradil protection group B) 100 渭 mol / L nicoradil 10 渭 mol / L glibenclamide antagonized the protective group. After 24 hours of intervention, the cell proliferation and the activity of SOD and caspase-3 were detected by CCK method to verify the apoptosis and protection of the cells. Tunel staining was used to detect the morphology of apoptosis and calculate the apoptotic rate of cardiac myocytes in each group. Results: (1) compared with the control group, the proliferation of the cells in each experimental group decreased, the phenomenon of apoptosis was serious. Nicorandil inhibited the degree of apoptosis of the cells in a concentration dependent manner; (2) compared with the control group, The activity of SOD of CCK-8 OD450 渭 m was decreased, the activity of caspase-3 was decreased with the increase of concentration, and the apoptosis of Tunel was decreased with the increase of concentration. (3) the activity of SOD in CCK-8 OD450 渭 m of fluctuating high glucose nicordil glibenclamide group was lower than that of fluctuating apoptosis group and low concentration of nicorandiol group, and the activity of SOD in CCK-8 OD450 渭 m group was lower than that in volatile apoptotic group. The activity of Caspase-3 and the rate of apoptosis were higher than those of medium and high concentrations of nicorandil. The results were contrary to those of SOD. Conclusion: volatile high glucose can damage cardiomyocytes and induce apoptosis, and nicorandil can protect cardiomyocytes in a concentration-dependent manner, and its mechanism may be the opening of K-ATP channels.
【学位授予单位】：山西医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R54

【参考文献】