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目的 探讨利拉鲁肽(LIRA)对高糖诱导的H9c2细胞凋亡的影响.方法 在H9c2细胞的高糖培养液中加入LIRA、活性氧簇分子(ROS)清除剂N-乙酰半胱氨酸(NAC)、p38丝裂原活化蛋白激酶(p38MARK)抑制剂SB203580和c-Jun氨基末端激酶(JNK)抑制剂SP600125等不同的处理因素作用24h,采用流式细胞术检测细胞的凋亡,采用Western blot法检测H9c2细胞活化的含半胱氨酸的天冬氨酸蛋白水解酶3(c-caspase-3)、丝裂原活化蛋白激酶(MAPK)家族磷酸化的p38MAPK(p-p38MAPK)和JNK(p-JNK)的蛋白水平.结果 正常糖对照组、等渗透压对照组和高糖组(HG组)的细胞凋亡率分别为(1.04±0.11)%、(1.27±0.04)%和(28.60±1.08)%.与正常糖对照组比较,等渗透压对照组的细胞凋亡率差异无统计学意义(P>0.05),而HG组的细胞凋亡率显著增加(P<0.01).HG+ LIRA组、HG+ NAC组、HG+ SB203580组和HG+ SP600125组的细胞凋亡率分别为(6.67±0.77)%、(3.65±0.26)%、(4.59±0.48)%和(4.22±0.89)%.与HG组比较,HG+ LIRA组、HG+ NAC组、HG+ SB203580组和HG+ SP600125组的凋亡率均明显下降(P<0.01).与正常糖对照组比较,HG组心肌细胞内c-caspase-3、p-p38MAPK和p-JNK的蛋白表达水平明显上升(P<0.01).与HG组比较,利拉鲁肽明显抑制了c-caspase-3蛋白水平(P<0.01),降低了p-p38MAPK和p-JNK的蛋白表达水平(P 0. 05 ) ,and the rate of apoptosis in HG group increased significantly( P < 0. 01 ). Compared with HG group, cell apoptosisin HG + LIRA group, HG + NAC group, HG + SB203580 group and HG+SP600 125 group decreased significantly (P < 0. 01 ). Compared with the control group, the c-caspase-3 ,p-p38MAPK and p-JNK protein levels increased significantly in the HG group (P < 0.01 ). Compared with HG group, liraglutide significantly reduced the c-caspase-3, p-p38MAPK and p-JNK protein expression levels. Conclusion Liraglutide may inhibit high glucose-induced apoptosis in H9c2 cardiomyocyte through the inhibition of phosphorylation of p38MAPK and JNK.