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目的观察吡格列酮对糖基化终产物(AGEs)刺激下大鼠血管平滑肌细胞(VSMCs)增殖的作用及对过氧化物酶体增殖物激活受体γ(PPARγ)基因及蛋白表达水平的影响,探讨PPARγ在AGEs诱导VSMCs增殖中的作用。方法(1)MTT法观察不同浓度、不同时间的AGEs对VSMCs增殖的影响及吡格列酮(1.0、10、100μmol/L)与AGEs共孵育对VSMCs增殖的干预作用。(2)用半定量逆转录聚合酶链反应测定VSMCs中PPARγmRNA的表达。(3)用Western blot法检测PPARγ的蛋白表达。结果AGEs作用导致VSMCs增殖,AGEs抑制PPARγmRNA和蛋白表达水平,这种抑制作用随着AGEs干预的时间延长和浓度的增加而增强(P<0.05)。PPARγ激活剂吡格列酮通过增加PPARγ的表达,抑制AGEs诱导的VSMCs增殖。结论PPARγ表达的下降可能是糖尿病易患动脉粥样硬化的重要原因之一。
Objective To investigate the effect of pioglitazone on the proliferation of vascular smooth muscle cells (VSMCs) and the expression of peroxisome proliferator - activated receptor The Role of PPARγ in Proliferation of VSMCs Induced by AGEs. Methods (1) MTT assay was used to observe the effects of different concentrations of AGEs on the proliferation of VSMCs and the effects of pioglitazone (1.0, 10, 100μmol / L) and AGEs on the proliferation of VSMCs. (2) The expression of PPARγmRNA in VSMCs was determined by semi-quantitative reverse transcription polymerase chain reaction. (3) Western blot was used to detect the protein expression of PPARγ. Results AGEs resulted in the proliferation of VSMCs. AGEs inhibited the mRNA and protein expression of PPARγ. The inhibitory effect of AGEs was enhanced with the prolongation of AGEs and the concentration of AGEs (P <0.05). Pioglitazone, a PPARγ activator, inhibits AGEs-induced proliferation of VSMCs by increasing PPARγ expression. Conclusion The decreased expression of PPARγ may be one of the important causes of atherosclerosis in diabetic patients.