【摘要】 目的探讨血管紧张素Ⅱ(Angiotensinll,Angll)是否通过调控血管外膜过氧化氢酶(Catalase,CAT)促进血管重塑。方法培养大鼠胸主动脉外膜成纤维细胞,分为对照组、Angll组、PD98059(ERK1/2抑制剂)组、Angll+PD98059组,取4~7代用于实验;使用含10~7mol/LAng ll的DMEM培养液分别刺激成纤维细胞0、0.5、2、6、12、24h,研究AngⅡ对CAT作用的时间关系;分别以0、10~8、10~7、10~6、10~5 mol/L的Angll刺激成纤维细胞24h,研究Ang ll对CAT作用的浓度关系;采用PD98059(ERK1/2抑制剂),研究ERK1/2信号通路对CAT表达的影响。结果 Angll能够显著下调CAT的表达,并呈时间和剂量依赖性;Angll能够通过ERK1/2信号通路下调血管外膜CAT的表达,阻断ERK1/2信号通路能够恢复CAT的表达。结论 Angll可能通过ERK1/2信号通路下调血管外膜CAT的表达,进而促进血管重塑的发生,导致血管病理性重塑发生。更多还原

【Abstract】 Objective To investigate the effect of ANG Ⅱ on vascular remodeling and its relation to regulation of adventitia catalase.Methods Adventitia fibroblasts were collected from rat thoracic aorta.The cultured adventitia fibroblasts were treated with ANG Ⅱ,PD 98059(ERK1/2 inhibitor) or ANG Ⅱ with PD98059,respectively.Fibroblasts were treated with 10~7mol/L ANG Ⅱ for0,0.5,2,6 and 24h;or with 0,10~8,10~7,10~6,10~5mol/L ANG Ⅱ for 24 h.The catalase(CAT) contents in culture supernatants were measured.Results ANG Ⅱ remarkably decreased CAT contents in a time-dose dependent manner.Blockage of ERK1/2 signal pathway by PD98059 increased the expression of CAT in adventitial fibroblasts.Conclusion ANG Ⅱ can down-regulate the adventitia CAT through ERK1/2 signal pathway,which leads to the vascular remodeling.更多还原