【摘要】：目的:探討尼可地爾(Nicorandial)對波動性高糖誘導的大鼠心肌細胞(H9C2)凋亡的抑制作用,驗證損傷與保護的可能的機制。方法:H9C2低糖培養(yǎng)基培養(yǎng)貼壁后進行分組,分別為A:低糖對照組;實驗組B:波動性高糖組(B0:波動性高糖凋亡組;B1:波動性高糖+10μmol/L尼可爾保護組;B2:波動性高糖+50μmol/L尼可地爾保護組;B3:波動性高糖+100μmol/L尼可地爾保護組B);C:波動性高糖+100μmol/L尼可地爾+10μmol/L格列苯脲拮抗保護組。分別干預24小時后,應用CCK法檢測各組細胞增殖情況;SOD活性、caspase-3活性驗證細胞凋亡及保護;應用TUNEL法染色檢測各組心肌細胞的凋亡形態(tài)以及計算凋亡率。結果:(1)與對照組相比,各實驗組細胞增殖減少,凋亡現(xiàn)象嚴重,尼可地爾可抑制細胞的凋亡程度,且呈濃度依賴性;(2)與對照組相比,加不同濃度尼可地爾保護各組細胞CCK-8 OD450μm、SOD活性均降低,隨濃度升高降低幅度減少,Caspase-3活性升高,隨濃度上升增高幅度減少,TUNEL染色細胞凋亡增多,呈濃度依賴性;(3)波動性高糖+尼可地爾+格列苯脲心肌組CCK-8 OD450μm、SOD活性均降低較波動性凋亡組及低濃度尼可地爾保護組低,較中高濃度尼可地爾保護組高,Caspase-3活性及細胞凋亡率結果與SOD活性結果相反。結論:波動性高糖具有損傷心肌細胞的作用,可誘導其凋亡;尼可地爾具有心肌細胞保護的作用,且呈現(xiàn)濃度依賴性,其機制可能為K-ATP通道開放的作用。
[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.
【學位授予單位】：山西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R54

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