Protective Effects Of Aloperin On Monocroline-induced Pulmonary Hypertension In Rats

Objective The purpose of this study was to investigate the effects of aloperine on monocrotaline-induced pulmonary hypertension in rats and To investigate the protective effect of aloperine on monocrotaline-induced pulmonary hypertension in rats and its relationship with regulation of Rho A / ROCK signaling pathway.Methods1.The mean pulmonary artery pressure and right ventricular systolic pressure in rats with pulmonary hypertension were measured by cardiac function analyzer.2.Effects of aloperine on pathological changes of lung tissue in pulmonary hypertension rats by HE Staining.3.Effects of aloperine onpulmonary artery acceleration time in rats with pulmonary hypertension by echocardiography.4.The effect of aloperine on the expression of ?-SMA and PCNA in pulmonary arteries of pulmonary hypertension rats was detected by immunohistochemical staining.5.The effects of ALO on the expression of Rho A,ROCK1,ROCK2,t-MYPT1,p-MYPT1,p27kip1,Bax and Bcl-2 protein in lung tissue of rats with pulmonary hypertension were detected by Western blot.6.RT-q RCR was used to detect the effect of ALO on the expression of Rho A,ROCK1 and ROCK2 m RNA in lung tissue of rats with pulmonary hypertension.Result1.Compared with the normal group,the mean pulmonary arterial pressure(P <0.05)and right ventricular systolic pressure(P <0.05)were significantly higher in the model group than in the model group(P <0.05)(P <0.05)and right ventricular systolic pressure(P <0.05).2.The results of H.E.staining showed that the administration of paclitaxel(25,50,100 mg / kg)could reduce the pathological changes of pulmonary tissue after pulmonary hypertension,significantly reduce the percentage of pulmonary vascular wall thickness(P <0.05)and blood vessel Wall area percentage(P <0.05).3.The results of echocardiography showed that the time of blood flow was significantly lower in the group(50,100 mg / kg)compared with the model group(P <0.05).4.Compared with the model group,the expression of ?-SMA(P <0.05)and PCNA(P <0.05)in the pulmonary arteries of pulmonary hypertension were significantly lower than that in the control group(50,100 mg / kg).5.Western blot analysis showed that Rho A(P <0.05),ROCK1(P <0.05),ROCK2(P <0.05),Bcl-2(P <0.05)and p-(P <0.05),ROCK1(P <0.05),ROCK2(P <0.05),and the expression of MYPT1(P <0.05)was significantly higher than that of model group(P <0.05)),Bcl-2(P <0.05)and p-MYPT1(P <0.05),and significantly increased the expression of p27kip1(P <0.05)and Bax(P <0.05),but had no effect on the expression of t-MYPT1.6.RT-q PCR results showed that the expression of Rho A(P <0.05),ROCK1(P <0.05)and ROCK2(P <0.05)m RNA in the lung tissue of the model group were significantly higher than those in the normal group(P <0.05),ROCK1(P <0.05)and ROCK2(P <0.05)m RNA expression were significantly decreased by berberine(100 mg / kg).Conclusion 1.ALO has protective effects on monocrotaline-induced pulmonary hypertension.2.The protective effect of ALO on monocrotaline-induced pulmonary hypertension in rats is related to the regulation of Rho A / ROCK signaling pathway.