利拉鲁肽对缺氧/复氧诱导的乳鼠心肌细胞损伤的影响

目的]观察新型降糖药物利拉鲁肽对缺氧/复氧(H/R)诱导的乳鼠心肌细胞损伤的影响.方法]将体外培养Wistar大鼠乳鼠心肌细胞进行分组:单纯H/R组(A组)、利拉鲁肽组+H/R组(B组)、正常对照组(C组),将A,B两组细胞同时进行H/R损伤,复氧后分别检测3组的乳酸脱氢酶(LDH)、丙二醛含量(MDA)、超氧化酶歧化酶(SOD)活性及各组心肌细胞凋亡率.结果]A组与C组比较,其细胞培养液中LDH、MDA含量、细胞凋亡率均增加,SOD活性降低,且差异有显著性(P＜0.01).与A组相比,B组LDH、MDA含量、细胞凋亡率则明显降低(P＜0.01),但仍高于C组,且差异有显著性(P＜0.01);SOD活性较A组增高,差异亦有显著性(P＜0.01).结论]H/R可以造成心肌细胞的损伤,增加细胞的凋亡;利拉鲁肽作为胰高血糖素样肽-1类似物,其直接作用于心肌细胞,可减轻H/R造成的心肌细胞损伤,抑制心肌细胞的凋亡,具有潜在的心脏保护作用.

Effects of Liraglutide on the Injury of Neonatal Rat Cardiomyocytes Induced by Hypoxia /Reoxygenation

Objective]To observe the effects of a new antidiabetic drug Liraglutide on injury of neonatal rat cardiomyocytes induced by hypoxia / reoxygenation(H/R).Method] Wistar rat myocardial cells were cultured in vitro and were divided into three groups:simple H/R group(group A),Liraglutide + H/R group (group B),and normal control group (group C).In addition to the normal control group,the remaining two groups were injured by H/R.Dehydrogenase (LDH),malondialdehyde (MDA) levels,superoxide dismutase (SOD) activity,and apoptotic cardiomyocytes were detected in the three groups.Results]Compared with group C,MDA,LDH levels,and apoptosis rate in group A were significantly higher,and the activity of SOD was lower (P ＜0.01).Compared with group A,the LD H,MDA level,and cell apoptosis rate in group B was significantly lower (P ＜0.01),but was still higher than those in group C (P ＜0.01).Compared with groups B and C,the SOD activity was significantly higher in group A (P ＜0.01).Conclusion]H/R can damage of myocardial cells and increase cell apoptosis.As glucagon like peptide-1 analogue,Liraglutide shows potential cardioprotective effects by directly acting on myocardial cells,which includes reducing myocardial cell injury and inhibiting the apoptosis caused by H/R.