微创医学

目的观察瑞舒伐他汀对左向右分流肺动脉高压大鼠肺血管重构、肺动脉平滑肌细胞凋亡以及bcl-2蛋白表达的影响,研究瑞舒伐他汀拮抗肺高血流性肺动脉高压的可能机制。方法 36只SD大鼠随机分为分流给药组、分流组、对照组,观察各组大鼠平均肺动脉压(mPAP)、右室肥厚指数(RVI)、肺小动脉中膜厚度百分比(WT)、肺小动脉管壁面积百分比(WA)的变化,TUNEL法检测大鼠肺动脉平滑肌细胞凋亡情况,Western Blot法检测大鼠肺组织中凋亡抑制蛋白bcl-2的表达情况。结果分流给药组较分流组大鼠mPAP、RVI、WT、WA值均有所下降,分流给药组大鼠凋亡的肺动脉平滑肌细胞明显增多,而bcl-2蛋白的表达减弱。结论瑞舒伐他汀能明显抑制肺高血流性模型大鼠肺动脉压力升高及肺血管重构,而抑制大鼠肺组织中bcl-2蛋白的表达,促进肺动脉平滑肌细胞凋亡是其可能的机制。

Objective To observe the effect of rosuvastatin on pulmonary artery remodeling，apoptosis of PASMCs and bcl-2 protein expression in rats with left to right shunt pulmonary hypertension and explore the mechanism of rosuvastatin against left to right shunt pulmonary hypertension． Methods 36 rats were randomly divided into 3 groups: shunt + rosuvastatin group，shunt group and control group． We observed the changes of mPAP，RVI，WT and WA of rats． Protein expression of bcl-2 in rats were measured by Western Blot and apoptosis of PASMCs was measured by TUNEL assay． Results Rats of shunt + rosuvastatin group presented with reducing of mPAP，RVI，WT，WA together with decreasing of bcl-2 protein and increasing of apoptotic PASMCs at 11th week in comparison with rats of shunt group． Conclusion Rosuvastatin can effectively inhibit the elevation of mPAP and remodeling of pulmonary artery． It maybe relate with down-regulating expression of bcl-2 protein and accelerating apoptosis of PASMCs in rats．

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