论文部分内容阅读
目的:研究胰高血糖素样肽-1(glucagon-like peptide-1,GLP-1)对缺氧/复氧(H/R)诱导的乳鼠心肌细胞损伤的影响及其可能的机制。方法:将体外培养乳鼠心肌细胞分为3组,即正常对照组、H/R组和GLP-1+H/R组。H/R损伤后,分别通过比色法、流式细胞术、荧光检测法测定上清液中乳酸脱氢酶(LDH)的活性、心肌细胞的凋亡率及半胱氨酸天冬氨酸特异性蛋白酶-3(caspase-3)的活性。结果:与正常对照组比较,H/R组LDH的活性、心肌细胞的凋亡率及caspase-3的活性均明显增高(P<0.01);而与H/R组相比,GLP-1+H/R组LDH的活性、心肌细胞的凋亡率及caspase-3的活性则明显降低(P<0.01)。结论:GLP-1可直接作用于心肌细胞,对H/R诱导的心肌细胞损伤产生一定的拮抗作用,其作用机制可能主要是通过抑制心肌细胞的凋亡所致;而GLP-1对心肌细胞凋亡的抑制作用,可能与其对caspase-3相关的凋亡或抗凋亡途径的调节有关。
AIM: To investigate the effect of glucagon-like peptide-1 (GLP-1) on neonatal rat cardiomyocyte injury induced by hypoxia / reoxygenation (H / R) and its possible mechanism. Methods: The neonatal rat cardiomyocytes were divided into 3 groups: normal control group, H / R group and GLP-1 + H / R group. After H / R injury, the activity of lactate dehydrogenase (LDH) in supernatant, the apoptosis rate of cardiomyocytes and the activity of cysteine aspartate Specific proteinase-3 (caspase-3) activity. Results: Compared with the normal control group, the activity of LDH, the apoptosis rate of cardiomyocytes and the activity of caspase-3 in H / R group were significantly increased (P <0.01). Compared with H / R group, the activities of GLP- The activity of LDH, the apoptosis rate of cardiomyocytes and the activity of caspase-3 in H / R group were significantly decreased (P <0.01). CONCLUSION: GLP-1 can act directly on cardiomyocytes and antagonize cardiomyocyte injury induced by H / R. The mechanism may be mainly through inhibiting the apoptosis of cardiomyocytes. However, GLP-1 inhibits cardiomyocytes The inhibitory effect of apoptosis may be related to its regulation of caspase-3-related apoptosis or anti-apoptotic pathway.