Osthole attenuates the right ventricle remodeling induced by MCT through up-regulated the expression

来源 :中国药理学会抗炎免疫药理专业委员会第十一届全国学术会议 | 被引量 : 0次 | 上传用户:zouximu19840420
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  Aim To investigate the effect of Osthole (Ost) on the right ventricle(RV) remodeling induced by monocrotaline (MCT) in rats and explore the mechanism.Methods Forty-five male Sprague-Dawley rats of 200~220g were randomly divided into normal control group (n=10), model group (n=1 5), low dose of Ost treatment group (10 mg·kg-1, n=10) and high dose of Ost treatment group (20 mg·kg-1, n=10).All rats were adaptability raised a week, then three groups of rats were given a single dose of MCT (50 mgkg-1) subcutaneously to establish the RV remodeling model.The rats in the Ost treatment group were administered (ig, qd) from 1 day to 28 days.The other rats in the model group and control group were given the same amount of ddH2O.All animals were sacrificed after 28 days of administration.The RV was weighed and the relative weight ratio of RV to the left ventricle with septum weight (LV+SEP) was calculated.The morphological changes of the RV was observed by light microscope and transmission electron microscope.The protein expression of PPAR-γ and IκB were detected by western blotting.Results Compared with the normal control group, the weight were lost and the RVHI was significantly increased (P<0.01) in model group.The RV myocardial hypertrophy, and the swollen mitochondria and the sarcoplasmic reticulum were obviously in model group.The protein expression of PPAR-γ and IκB in RV tissues were down-regulated in model group (P<0.01).Compared with the model group, weight lost and the value of RV weight index (P<0.01 or P<0.05), the RV myocardial hypertrophy, the swollen mitochondria and the sarcoplasmic reticulum were improved significantly, as well as the protein expression of PPAR-γ and Iκ B in RV tissues were up-regulated (P<0.01 or P<0.05) in Ost treatment group.Conclusion Ost attenuates the development of right ventricle remodeling induced by MCT in rats, and the mechanism might be related to up-regulated the expression of PPAR-γ and IκB.
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