摘要
目的观察辛伐他汀对野百合碱（MCT）诱导的肺动脉高压大鼠血管细胞粘附分子-1（VCAM．1）表达的影响，探讨辛伐他汀治疗肺动脉高压的作用机制。方法将30只健康雄性SD大鼠随机平均分为正常对照组（Con组），MCT诱导的肺动脉高压组（MCT组），辛伐他汀干预治疗组（SS组）。MCT组和SS组注射野百合碱造模，ss组采用辛伐他汀干预治疗。治疗3周后，采用右心导管法检测大鼠平均肺动脉压（mPAP）；称量RV和LV＋s，计算右心肥大指数（RVHI）。肺组织切片进行苏木素-伊红（HE）染色，光镜下观察肺组织形态学的改变。采用RT-PCR和免疫组化法检测肺组织中VCAM-1 mRNA和蛋白质的表达情况。结果ss组大鼠的mPAP和RVHI较MCT组均明显降低（P〈0．01），SS组大鼠肺中小动脉管壁厚度较MCT组减小，管腔面积增大，血管周围炎明显减轻。SS组大鼠肺组织中VCAM-1mRNA的表达显著低于MCT组，肺组织中VCAM-1阳性细胞积分低于MCT组，但明显高于Con组。结论辛伐他汀可有效降低肺动脉压、改善肺血管重构，其机理可能与抑制肺组织VCAM-1的表达有关。
Objective To study the effects of simvastatin on the expression of vascular cell adhesion molecule-1 （ VCAM-1 ） in monocrotaline （MCT）- induced pulmonary hypertension rats, and investigate the therapeutic mechanism of simvastatin to pulmonary hypertension. Methods 30 SD rats were divided into 3 groups, normal control group （ Con group） , MCT -induced pulmonary hypertension group （MCT group） and simvastatin treatment group （SS group）. The rats in control group and therapeutic group were injected to induced pulmonary hypertension with MCT. After 3 weeks, the mean pulmonary arterial pressure （mPAP） and fight ventricular hypertrophy index （RVHI） were measured, and the expression of VCAM-1 mRNA and protein in lung tissues were detected by RT-PCR and immunohistoehemistry, respectively. Results mPAP, RVHI and the expression of VCAM-1 in lung tissues in MCT group were higher than those in Con group and SS group. Moreover, mPAP, RVHI and the expression of VCAM-1 in lung tissues had no difference between SS group and Con group. Conclusion Simvastatin has therapeutic effect on pulmonary hypertension through down-regulating the expression of adhesion molecule VCAM-1.
出处
《中国医师杂志》
CAS
2009年第8期1045-1048,共4页
Journal of Chinese Physician
