水飞蓟素对野百合碱诱发肺动脉高压大鼠肺血管重构的保护作用

Protective effect of Silymarin on rats with monocrotaline induced pulmonary hypertension

目的探讨水飞蓟素对野百合碱(MCT)诱发肺动脉高压大鼠模型肺血管重构的保护作用及机制。方法 24只雄性SD大鼠随机分为正常对照组(C组)、MCT诱发肺动脉高压模型组(M组)、水飞蓟素治疗组(S组),每组8只。28d后,右心导管法测量各组右心室收缩压(RVSP),称量法计算右心室肥大指数(RVHI),HE染色和α-平滑肌肌动蛋白(α-SMA)免疫组织化学染色观察肺血管重构,TUNEL法检测肺动脉平滑肌细胞凋亡,RT-PCR法行肺组织Fas mRNA半定量检测。结果与M组比较,S组RVSP、RVHI、α-SMA表达均降低(P<0.01),肺动脉平滑肌细胞凋亡稍升高,肺组织Fas mRNA表达升高(P<0.05)。结论水飞蓟素对野百合碱诱发肺动脉高压大鼠肺血管重构具有保护作用。

Objective To investigate the protective effects of silymarin on rats with monocrotaline induced pulmonary hypertension and explore its therapeutic mechanism.Methods 24 male SD rats were randomly divided into 3 groups,the control group（n=8）,the pulmonary hypertension model group（n=8） and the silmymarin treatment group（n=8）.Right ventricular systolic pressure（RVSP） were detected by right heart catheter after twenty-eight days.Right ventricular hypertrophy index（RVHI） was calculated as the right ventricle to the left ventricular plus septum weight.With HE staining,immunohistochemical analysis of α-smooth muscle actin（α-SMA） to observe pulmonary artery structural changes.The pulmonary artery smooth muscle cells apoptosis were detected by TUNEL.The expression of Fas mRNA in the pulmonary tissue was detected by RT-PCR.Results Compared with the model group,silymarin treatment group decreased RVSP,RVHI and α-SMA,increased apoptosis of pulmonary artery smooth muscle cells and Fas mRNA.Conclusion Silymarin could protect rats with monocrotaline induced pulmonary hypertension.