阿托伐他汀在实验性肺动脉高压中的作用机制  

Study on the mechanism of atorvastatin for experimental pulmonary hypertension

作　　者：唐丽[1] 吴尚洁[2] 邢西迁[2] 甘烨[2] 

机构地区：[1]湖南省第二人民医院,长沙市410007 [2]中南大学湘雅医学院附属二医院,长沙市410007

出　　处：《实用医学杂志》2011年第12期2131-2133,共3页The Journal of Practical Medicine

摘　　要：目的:观察阿托伐他汀对大鼠实验性肺动脉高压的治疗效果,探讨其可能治疗机制。方法:将SD大鼠随机分为正常对照组、肺动脉高压模型组(MCT组)、阿托伐他汀干预组(AS组)。测定大鼠平均肺动脉压(mPAP)和右心室肥大指数(RVHI)。采用免疫组化法测定大鼠肺血管内皮p38 MAP激酶(p38 MAPK)的表达。结果:与MCT组比较,AS组大鼠的mPAP、RVHI和p38 MAPK的表达均明显降低(均P<0.01)。结论:阿托伐他汀能减轻野百合碱诱导的大鼠肺动脉高压,有可能通过抑制肺血管内皮p38 MAPK的表达而实现。Objective To observe the effect of atorvastatin on experimental pulmonary hypertension in rats and to explore its mechanism. Methods SD rats were randomly divided into 3 groups： control group, MCT group and atorvastatin group （AS group ）.Mean pulmonary arterial pressure （mPAP） and fight ventricular hypertrophy index （1RVHI） were measured;The expression of p38 MAPK in lung was observed by immunohistochemistry. Results Comparing with MCT group, the mPAP, the RVHI and The expression of p38 MAPK in pulmonary vascular endothelial cells in AS group were all decreased significantly （P 〈 0.01 ）. Conclusions Atorvastatin could inhibit MCT-induced p38 MAPK expression of pulmonary vascular endothelial cells and the development of pulmonary hypertension.

关 键 词：肺动脉高压 P38 MAP激酶 阿托伐他汀 

分 类 号：R965[医药卫生—药理学]