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缬沙坦对血管平滑肌细胞迁移及丝裂原活化蛋白激酶的影响 被引量:1

Valsartan on migration of vascular smooth muscle cell via MAPK pathway
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摘要 目的观察缬沙坦(Val)对血管紧张素Ⅱ(AngⅡ)刺激下大鼠血管平滑肌细胞(VSMC)迁移及磷酸化42/44丝裂原活化蛋白激酶(p42/44MAPK)表达的影响。方法组织贴块法培养大鼠胸主动脉平滑肌细胞,tran-swell小室检测细胞的迁移能力,免疫印迹法检测p42/44 MAPK蛋白表达的水平。结果(1)AngⅡ能明显促进VSMC迁移,该作用可被Val和MAPK激酶的特异性抑制剂PD98059所抑制。(2)AngⅡ刺激VSMC 5min时,p42/44 MAPK的表达量最大,该作用可被Val和PD98059所抑制。(3)Val单独作用于VSMC时,对细胞的迁移及p42/44 MAPK的表达均无明显影响。结论Val抑制AngⅡ诱导的VSMC迁移与其抑制AngⅡ诱导的p42/44MAPK的表达相关。 Objective To determine the effect of valsartan(val) on the migration of isolated rat vascular smooth muscle cell(VSMC) and the expression of phospho-42/44 mitogen-activated protein kinase(p42/44 MAPK) promoted by angiotensin Ⅱ. Methods VSMC from the rat thoracic aorta was cultured by attachment-block culture. VSMC migration was measured by migration chamber system, p42/44 MAPK expression was determined hy Western blot. Results (1) Angiotensin Ⅱ obviously promoted VSMC migration, the effect was inhibited by valsartan and PD98059. (2)Angiotensin Ⅱ obviously promoted p42/44 MAPK expression,and the expression was at maximal in 5 min,the effect was inhibited by val and PD98059. (3)Compared with the control, val didn't inhibit VSMC migration and p42/44 MAPK expression. Conclusion The effect that val inhibits angiotensin Ⅱ-induced VSMC migration is related to its inbibiting angiotensin Ⅱ-induced p42/44 MAPK expression.
出处 《中华老年多器官疾病杂志》 2009年第4期364-367,369,共5页 Chinese Journal of Multiple Organ Diseases in the Elderly
基金 教育部博士点基金(20050025012)
关键词 平滑 血管 缬沙坦 血管紧张素Ⅱ 丝裂原活化蛋白激酶 muscle, smooth, vascular valsartan angiotensin Ⅱ mitogen-activated protein kinase
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