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目的研究罗格列酮(RGZ)对高浓度葡萄糖(高糖)孵育下的血管平滑肌细胞(VSMCs)增殖和凋亡的影响。方法 VSMCs取自大鼠胸主动脉。MTT法检测细胞增殖活性,流式细胞术检测VSMCs细胞周期、凋亡率及Bcl-xl、Bcl-2蛋白表达,Western blot检测VSMCs Bcl-x1蛋白表达。结果高糖(Glu 11.2、22.4 mmol/L)培养可明显促进VSMCs增殖,抑制其凋亡;30及100 μmol/LRGZ以浓度依赖形式抑制高糖孵育下VSMCs增殖活性,阻止其由G_0/G_1期向S期转变,降低VSMCs Bcl xl、Bcl-2表达,并促进其凋亡;RGZ拮抗剂GW9662预处理可部分拮抗RGZ的作用。结论 RGZ可通过对细胞周期的干预,抑制高糖诱导的VSMCs增殖,下调Bcl-xl、Bcl-2表达,促进VSMCs凋亡,在2型糖尿病大血管病变的防治中发挥重要作用。
Objective To investigate the effects of rosiglitazone (RGZ) on the proliferation and apoptosis of vascular smooth muscle cells (VSMCs) incubated with high glucose (high glucose). Methods VSMCs were obtained from the thoracic aorta of rats. Cell proliferation was detected by MTT assay. Cell cycle, apoptosis rate and expression of Bcl-xl and Bcl-2 were detected by flow cytometry. Bcl-x1 protein expression was detected by Western blot. Results Cultured with high glucose (11.2,22.4 mmol / L) significantly increased the proliferation and inhibited the apoptosis of VSMCs. The proliferation of VSMCs was inhibited by 30 and 100 μmol / L LRZ in a concentration-dependent manner, To S phase, reducing the expression of Bcl-xl and Bcl-2 in VSMCs, and promoting their apoptosis. The pretreatment with RGZ antagonist GW9662 could partially antagonize the effect of RGZ. Conclusion RGZ can inhibit the proliferation of VSMCs induced by high glucose, down-regulate the expression of Bcl-xl and Bcl-2, and promote the apoptosis of VSMCs through the intervention of cell cycle. It plays an important role in the prevention and treatment of type 2 diabetic macroangiopathy.