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目的探讨坎地沙坦(Cand)对高糖诱导的大鼠胸主动脉平滑肌细胞株A7r5增殖的影响及作用机制。方法体外培养A7r5细胞,分为对照组、高糖组、Cand(低、中、高)剂量组;通过CCK-8法检测细胞增殖活性,流式细胞术检测细胞周期,Western blot法检测p-c-Raf、p-MEK1/2、p-ERK1/2蛋白表达水平。结果与对照组比较,高糖组A7r5细胞增殖活性明显增强,细胞周期S期比例[(30.503±1.521)%]明显增加(P<0.01),A7r5细胞内p-c-Raf、p-MEK1/2、p-ERK1/2蛋白表达水平[分别为(1.060±0.087)、(1.155±0.064)、(1.924±0.065)]明显升高(P<0.05);与高糖组比较,Cand高剂量组A7r5细胞增殖活性下降,细胞周期S期比例[(21.677±1.690)%]下降(P<0.01),A7r5细胞内p-c-Raf、p-MEK1/2、p-ERK1/2蛋白表达水平[分别为(0.658±0.039)、(0.821±0.049)、(0.795±0.028)明显下降(P<0.01)。结论坎地沙坦对高糖诱导的A7r5细胞增殖具有抑制作用,其机制可能与抑制细胞周期及信号传导通路上3种蛋白磷酸化有关。
Objective To investigate the effect of candesartan on proliferation of rat aorta smooth muscle cell line A7r5 induced by high glucose and its mechanism. Methods A7r5 cells were cultured in vitro and divided into control group, high glucose group and Cand (low, medium and high) dose groups. Cell proliferation was detected by CCK-8 assay. Cell cycle was detected by flow cytometry. Raf, p-MEK1 / 2, p-ERK1 / 2 protein expression levels. Results Compared with the control group, the proliferation of A7r5 cells in high glucose group was significantly increased (P <0.01). The proportion of pc-Raf, p-MEK1 / 2, The expression of p-ERK1 / 2 protein in the high-glucose group (1.060 ± 0.087, (1.155 ± 0.064), (1.924 ± 0.065)] was significantly higher than that in the high glucose group The expression of pc-Raf, p-MEK1 / 2 and p-ERK1 / 2 in A7r5 cells were decreased (P <0.01) ± 0.039), (0.821 ± 0.049) and (0.795 ± 0.028), respectively (P <0.01). Conclusion Candesartan can inhibit the proliferation of A7r5 cells induced by high glucose. The mechanism may be related to the inhibition of the phosphorylation of the three proteins in the cell cycle and signal transduction pathway.