| objective To investigate the effect and mechanism of ethanol extract of Cyathula officinalis Kuan on pulmonary arterial hypertension induced by monocrotaline in rats.Methods randomly divide 48 SD rats into 6 groups(n=8): control group,MCT group,MCT+ the high(24g/kg),middle(12g/kg),low(6g/kg)dose of ethanol extract of Cyathula officinalis Kuan and Sildenafil treatment group(30mg/kg).The rats in the latter 5 groups were intraperitoneally injected with monocrotaline(60 mg/kg)to establish a pulmonary hypertension model,and the control group was injected with the same amount of normal saline.On the 28 th day of the injection of monocrotaline,the drug-administered group was given the corresponding ethanol extract of cyathula officinalis kuan and Sildenafil,the mean pulmonary artery pressure(mPAP)and right ventricular systolic pressure(RVSP)was measured in each group.Dtected the expression of MDA and the activity of SOD.Hematoxylin-eosin(HE)staining was used to observe and calculate the medial thickness index(WT)of pulmonaryarterioles and right ventricular hypertrophy index.Western blot was used to observe the expression of PI3K/Akt protein in rat lung tissue.Results The ratios of MCT group increased significantly(P <0.05)compared with the control group,the levels of PI3K/Akt protein,and mRNA expression were significantly higher(P<0.05)than the control group.The levels of PI3K/Akt protein and mRNA expression in the high and medium dose group and Sildenafil treatment group were significantly lower than MCT group(P<0.05).There were no significant(P>0.05)differences between the high and medium dose group and Sildenafil treatment group with the control group in mPAP,RVSP,RV/(LV+S)(%),WT(%)and the expression levels of PI3K/Akt protein and mRNA.The activity of SOD in the high,middle and low doses of Achyranthes bidentata L.was significantly higher than that of the control group,and the MDA content was significantly lower than that of the control group(P<0.05).Conclusion The ethanol extract of Cyathula officinalis Kuan can reduce the pulmonary hypertension induced by monocrotaline Inhibition of oxidative stress and reduce pulmonary vascular remodeling.The mechanism may be related to PI3K/Akt signaling pathway. |