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目的:探讨p38 MAPK在兔颈动脉外膜损伤致内膜病变氧化应激中的作用。方法:采用高脂饮食喂养及胶原酶消化+机械分离的方法,建立兔颈动脉外膜损伤致内膜病变的模型。测定术后不同时间点,对照组和阿托伐他汀组家兔血脂指标(TC,TG,LDL-C和HDL-C)、新生内膜面积(NIA)、活性氧物质(ROS)的产生情况,观察磷酸化p38 MAPK的表达及定位。结果:从颈动脉外膜损伤术后1 d始,ROS的产生和磷酸化p38 MAPK的表达即增加并持续至少28 d。阿托伐他汀干预后,与对照组比较,各时间点ROS的产生及磷酸化p38的表达均下调(P<0.05),TC及LDL-C的水平下降(P<0.05),新生内膜形成减少(P<0.05)。结论:氧化应激水平的升高和p38MAPK的持续激活,是血管外膜损伤致新生内膜形成的可能机制之一。
Objective: To investigate the role of p38 MAPK in oxidative stress induced by adventitia of rabbit carotid artery. Methods: The model of intimal lesions caused by carotid artery adventitia was established by feeding with high-fat diet and collagenase digestion + mechanical separation. The levels of TC, TG, LDL-C and HDL-C, NIA and ROS in rabbits in control group and atorvastatin group were measured at different time points after operation. , Observe the expression and localization of phosphorylated p38 MAPK. Results: From the first day after carotid artery injury, the production of ROS and the expression of phosphorylated p38 MAPK increased for at least 28 days. After atorvastatin intervention, ROS production and expression of phosphorylated p38 were down-regulated at each time point (P <0.05), TC and LDL-C levels were decreased (P <0.05), neointimal formation Decrease (P <0.05). CONCLUSION: The increase of oxidative stress and the sustained activation of p38MAPK are one of the possible mechanisms of neointimal formation induced by vascular adventitial injury.