摘要
【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。
[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.
出处
《医学临床研究》
CAS
2016年第12期2346-2348,共3页
Journal of Clinical Research
