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作 者:张乐[1] 邹军[1] 田风[1] 魏晓[1] 金鑫[1]
出 处:《中国生化药物杂志》2012年第6期709-712,共4页Chinese Journal of Biochemical Pharmaceutics
基 金:海峡(厦门)中医药科技平台项目(3502Z20100006);厦门市科技计划资助项目(3502Z20090009)
摘 要:目的研究油酰乙醇胺(OEA)对血管紧张素Ⅱ(AngⅡ)刺激大鼠主动脉血管平滑肌细胞(VSMCs)增殖的抑制作用以及对p38信号通路的影响。方法分离大鼠胸主动脉,组织贴块法培养VSMCs,AngⅡ刺激VSMCs建立细胞增殖模型,不同浓度OEA(5,10,20μmol/L)作用后,用溴脱氧核苷尿嘧啶(BrdU)掺入的方法检测细胞增殖活性;流式细胞术检测细胞周期变化;Western-bolt法检测对P-p38和p38蛋白表达的影响。结果与AngⅡ组比较,随着OEA浓度升高,VSMCs的增殖受到抑制、G0/G1比例显著升高,G2/M比例显著降低,且P-p38和p38蛋白的表达量降低并呈浓度依赖关系。结论 OEA对VSMCs的增殖有抑制作用,其机制可能是抑制了p38MAPK信号通路。Purpose To investigate the inhibitory effect of oleoylethanolamide on the proliferation of cultured rat vascular smooth muscle cells(VSMCs) induced by angiotensin II and the effect on p38 signa- ling pathway. Methods VSMCs were primary cultured by tissue sticking method. Cell proliferation model was established by stimulation with Ang II. After incubation with various concentrations of OEA(5,10,20 μmol/L) for 24 h, the proliferation effect was measured by using the BrdU cell proliferation assay kit. Cell cycle distribution was determined by flow cytometry analysis and the protein expression of P-p38 and p38 was assessed using Western blotting. Results Compared with the Ang lI group,along with the increased concentration of OEA,the proliferation of VSMCs was obviously inhibited, the cell ratio of G0/G1 phase obviously increased, and the cell ratio of G2/M phase significantly decreased. Besides, the expression of P-p38 and p38 protein decreased in a dose-dependent manner. Conclusion OEA had a inhibition on the proliferation of VSMCs,and might act by down-regulating p38MAPK pathway.
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