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肾上腺髓质素对血管紧张素Ⅱ诱导的血管外膜成纤维细胞增殖及转化的影响 被引量:1

Effects of adrenomedullin on angiotensin Ⅱ-induced vascular adventitial fibroblast proliferation and phenotypic transformation in vitro
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摘要 目的观察肾上腺髓质素(ADM)对血管紧张素Ⅱ的促成纤维细胞增殖及转化作用的影响。方法原代培养大鼠主动脉外膜成纤维细胞,随机分为对照组、ADM组、AngⅡ组及AngⅡ加不同浓度ADM(10-9~10-7mol/L)组。用四氮唑蓝(MTT)比色法测定细胞增殖活性,流式细胞分析仪检测细胞周期,蛋白免疫印迹法测定细胞内α-SMactin表达情况。结果与对照组相比,AngⅡ组S期和G2/M期细胞增多,MTTA值检测细胞增殖抑制率为-23.8%;ADM对基础水平的细胞周期中各期细胞构成比及细胞增殖抑制率并无明显影响;与AngⅡ组相比,AngⅡ加ADM组S期细胞构成比明显减少,细胞增殖抑制率提高了。经AngⅡ刺激后主动脉外膜成纤维细胞表达α-SMactin转变为肌成纤维细胞。ADM可抑制AngⅡ上述作用,下调α-SMactin表达。结论ADM对成纤维细胞的增殖及转化无明显影响,但ADM抑制AngⅡ诱导的血管成纤维细胞增殖及转化。 [Objective] To explore the effect of adrenomedullin on AngⅡ -induced proliferation and phenotypic transformation in cultured rat vascular adventitium fibroblasts (AF). [Methods] Rat vascular adventitial fibroblasts were cultured in vitro, cultured cells were incubated with AngⅡ, ADM and both. The cells proliferation was determined by MTT. Cell cycle analysis was performed by flow cytomertry. The expression of ix-SM actin in AF stimualted by different conditions was measured by Western blot. [Results] Compared with the control cells, AngII significantly increased the number of cells in S and GJM phase, cell proliferation inhibiting rate of MTT was -23.8%, whereas ADM had no such effect. The number of cells in S phase treated with both AngII and ADM was decreased, and the cell proliferation inhibiting rate was increased . During the course of the phenotypic transformation of myofibroblasts (MF) from AF induced by AngII, the expression of α-SM actin was significantly upregulated. ADM could inhibit AngII-induced expression of α-SM acfin in AF. [Conclusion] ADM does not influenced the proliferation and phenotypic tranformation of adventitial fibroblasts alone, but it markedly inhibits the AngⅡ role in stimulating proliferation and phenotypic tranformation of adventitial fibroblasts.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2008年第3期309-312,共4页 China Journal of Modern Medicine
关键词 肾上腺髓质素 血管外膜成纤维细胞 血管紧张素Ⅱ adrenomedullin vascular adventitial fibroblasts angiotensin Ⅱ
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