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目的探讨辛伐他汀(SIM)对高糖诱导的血管内皮细胞(VEC)增殖及凋亡的影响,及其对VEC保护的作用机制。方法将处于对数生长期的VEC随机分为正常对照组(Glu 5.5 mmol/L)、高糖组(Glu 33 mmol/L)、高糖+3个不同浓度SIM组,MTT法检测VEC增殖的变化,试剂盒检测细胞上清液中一氧化氮(NO)和内皮素(ET-1)的水平,流式细胞术检测各组细胞活性氧(ROS)的水平和凋亡率;增加高糖+SP600125组(SP600125 10.0μmol/L),Western blot法检测JNK蛋白表达和磷酸化水平。结果与正常对照组相比,高糖组细胞上清中NO水平明显下降、ET-1水平明显上升、ROS含量和凋亡率明显增加、JNK磷酸化水平明显上调。JNK抑制剂SP600125预处理后,VEC的p-JNK表达显著减少。SIM可显著逆转上述高糖效应,且呈一定的浓度依赖性。结论 SIM对VEC的保护作用可能与其促进细胞增殖、减少氧化应激和细胞凋亡、降低JNK的磷酸化水平有关。
Objective To investigate the effects of simvastatin on the proliferation and apoptosis of vascular endothelial cells (VECs) induced by high glucose and its mechanism of VEC protection. Methods VEC in the logarithmic growth phase were randomly divided into normal control group (Glu 5.5 mmol / L), high glucose group (Glu 33 mmol / L), high glucose + 3 different concentrations of SIM. MTT assay was used to detect VEC proliferation The levels of nitric oxide (NO) and endothelin (ET-1) in the cell supernatant were detected by the kit. The levels of reactive oxygen species (ROS) and apoptosis were detected by flow cytometry. + SP600125 group (SP600125 10.0μmol / L). The protein expression and phosphorylation of JNK were detected by Western blot. Results Compared with the normal control group, the level of NO in the supernatant of the high glucose group was significantly decreased, the level of ET-1 was significantly increased, the content of ROS and the apoptosis rate were significantly increased, and the phosphorylation of JNK was significantly increased. JNK inhibitor SP600125 pretreatment, VEC p-JNK expression was significantly reduced. SIM can significantly reverse the high glucose effect, and a certain concentration-dependent. Conclusions The protective effect of SIM on VEC may be related to the promotion of cell proliferation, the reduction of oxidative stress and apoptosis, and the decrease of phosphorylation of JNK.