摘要
目的观察辛伐他汀在野百合碱(MCT)诱导的肺动脉高压(PAH)大鼠模型中对Rho/Rock表达的影响,探讨辛伐他汀改善MCT所致PAH的机制。方法雄性SD大鼠30只随机均分为对照组、MCT模型组和辛伐他汀干预组(SS组)。测量各组大鼠干预后平均肺动脉压力(mPAP)、右心室肥厚指数(RVHI);观测大体的组织形态病理改变,采用免疫组化和Westernblot检测肺组织中的PCNA、α-SMA、Rho/Rock的表达。结果与对照组及干预组相比,MCT组的mPAP及RVHI显著增加(P<0.05),PCNA、α-SMA、Rho/Rock的表达显著增多(P<0.05);与对照组相比,SS组的mPAP及RVHI差异无统计学意义(P>0.05);而PCNA、α-SMA、Rho/Rock的表达显著增多(P<0.05)。结论辛伐他汀可有效减轻MCT诱导的PAH大鼠肺动脉压力,其机制可能与辛伐他汀通过Rho/Rock信号通路改善肺动脉平滑肌增生重构有关。
Objective This study was to discuss the effect of Simvastatin on pulmonary arterial pressure,expressions of Rho/ROCK in Monoerotaline （MCT）-induced pulmonary arterial hypertension （PAH） , discuss the mechanisms of simvastatin in improving pulmonary arterial remodeling. Methods 30 male SD rats were randomly divided into 3 groups： eontrol,MCT and Simvastatin （SS） groups （n = 10 in eaeh group）. The mPAP and RVHI of eaeh group was measured, the expressions of PCNA, α-SMA and Rho/Roek in lung tissues were detected by immunohistoehemistry staining and Western blot. Results Compared with the control group and SS group, the mPAP and RVHI in MCT group increased significantly （ P 〈 0.05 ） ; Meanwhile, the expressions of PCNA, α-SMA and Rho/Roek also increased significantly （ P 〈 0. 05）. Compared with the control group, the mPAP and RVHI in SS group did not increase significantly （ P 〉 0.05 ） ; but the expressions of PCNA, α-SMA and Rho/Rock increased significantly （ P 〈 0.05 ）. Conclusion Simvastatin can reduce pulmonary arterial pressure and reverse pulmonary vascular remodeling through Rho/Rock signal pathway.
出处
《中国分子心脏病学杂志》
CAS
2009年第4期199-203,共5页
Molecular Cardiology of China
作者简介
通讯作者：黄石安，E—mail：huangshian1969@yahoo．com．cn
