论文部分内容阅读
目的探讨利拉鲁肽对波动性高糖诱导的内皮细胞氧化损伤的影响及潜在机制。方法分离培养人脐静脉内皮细胞,分为正常葡萄糖对照(NC)组、持续性高糖(HG)组、波动性高糖(FG)组、高渗对照(HC)组、FG+利拉鲁肽(Lira)组、FG+Lira+Exendin(9-39)组和Exendin(9-39)组,各组均干预4d。采用流式细胞仪检测细胞内活性氧簇(ROS)水平和细胞凋亡比率,采用Western blot检测活化Caspase-3蛋白水平。结果与NC组相比,HG、FG组ROS水平升高[(129.4±4.1)%vs 100%;(130.5±1.2)%vs 100%,P<0.05],细胞凋亡比率增加[(21.6±1.7)%vs(14.8±3.9)%;(25.1±5.8)%vs(14.8±3.9)%,P<0.05],FG组活化Caspase-3蛋白水平升高[(223.6±2.4)%vs 100%,P<0.05]。与FG组相比,FG+Lira组ROS水平降低[(109.8±4.3)%vs(133.2±1.9)%,P<0.05],细胞凋亡比率降低[(17.3±3.9)%vs(26.5±4.2)%,P<0.05],活化Caspase-3蛋白水平降低[(110.3±6.4)%vs(223.6±2.4)%,P<0.05]。添加Exendin(9-39)可部分消除FG+Lira组的上述效应。结论利拉鲁肽抑制波动性高糖诱导的内皮细胞氧化损伤,其作用至少部分是呈GLP-1受体依赖性的。
Objective To investigate the effect of liraglutide on oxidative damage of endothelial cells induced by high glucose and its underlying mechanism. Methods Human umbilical vein endothelial cells were isolated and cultured and divided into normal glucose control (NC), continuous high glucose (HG), high glucose (FG), hypertonic (HC) and FG + (Lira group), FG + Lira + Exendin (9-39) group and Exendin (9-39) group. Each group was treated for 4 days. The levels of reactive oxygen species (ROS) and apoptosis were detected by flow cytometry. The protein level of Caspase-3 was detected by Western blot. Results Compared with NC group, ROS levels in HG and FG groups were significantly higher than those in NC group [(129.4 ± 4.1)% vs 100%; (130.5 ± 1.2)% vs 100%, P <0.05] 1.7% vs 14.8% ± 3.9%, 25.1 ± 5.8% vs 14.8 ± 3.9%, P <0.05]. The level of activated Caspase-3 protein in FG group was significantly higher than that in FG group [(223.6 ± 2.4)% vs 100% , P <0.05]. Compared with FG group, the level of ROS decreased in FG + Lira group [(109.8 ± 4.3)% vs (133.2 ± 1.9)% vs (17.3 ± 3.9)% vs (26.5 ± 4.2%, P <0.05] )%, P <0.05]. The level of activated Caspase-3 protein decreased (110.3 ± 6.4)% vs (223.6 ± 2.4)%, P <0.05]. The above effect of FG + Lira group was partially eliminated by adding Exendin (9-39). Conclusion Liraglutide inhibits oxidative damage of endothelial cells induced by high glucose and fluctuates at least partially in a GLP-1 receptor-dependent manner.