摘要
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 study the effects of glucagon-like peptide-1 （ GLP-1 ） on the injury of neonatal mice cardiomyocytes induced by hypoxia-reoxygenation （H/R） and to explore the possible mechanism. METHODS： Cultured neonatal mice cardiomyocytes were randomly divided into three groups： normal control group, H/R group, and H/R and GLP-1 group. LDH activity, apoptosis rate of cardiomyocytes and caspase-3 activity were detected. RESULTS： Compared with the normal control group, LDH activity, cardiomyocyte apoptosis rate and caspase-3 activity all increased significantly in the H/R group. Compared with the H/R group, the above three indexes all decreased in the I-I/R and GLP-1 groups. CONCLUSION： GLP-1 directly acts on cardiomyocytes and protects them from H/R injury mainly by inhibiting apoptosis. GLP-1 may exert its apoptotic effects through regulation of apoptotic or antiapoptotic pathways of caspase-3.
出处
《心脏杂志》
CAS
2010年第3期344-346,353,共4页
Chinese Heart Journal
