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Anluohuaxianwan Alleviates Carbon Tetrachloride-Induced Hepatic Fibrosis in Rats through Upregulation of Peroxisome Proliferator-Activated receptor-gamma and Downregulation of Nuclear Factor-Kappa B/IκBα Signaling Pathway

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World Journal of Traditional Chinese Medicine 2019年第2期5卷 95-103页

作者： Lin Wang Wei Lu Yu-Hua Gao Hai-Jiang Yan Fei Pei Xue-En Liu Hui Zhuang Departments of Microbiology and Center of Infectious Diseases School of Basic Medical Sciences Peking University Health Science CenterBeijing Department of Clinical Laboratory The First Affiliated Hospital of Zhengzhou UniversityZhengzhouChina Departments of Pathology School of Basic Medical SciencesPeking University Health Science CenterBeijing

Objective:The aim of this study was to investigate the effects of traditional Chinese medicine Anluohuaxianwan(ALHXW)on peroxisome proliferator-activated receptor-gamma(PPARγ)and nuclear factor-kappa B(NF-κB)signaling pathways using a rat model of carbon model groups were gavaged with saline for 6 weeks.Liver function was measured,and liver fibrosis and necroinflammation were assessed.Protein and messenger RNA expression levels of PPARγ,NF-κB,and Inhibitorαof NF-κB(IκBα)were analyzed by Western blot and reverse transcription–quantitative polymerase chain reaction.Results:ALHXW markedly alleviated liver injury compared with the model group,as indicated by the improvements in disease status,the morphology of liver and spleen,the liver and spleen indexes,and liver function.The extent of liver fibrosis was improved,hepatic stellate cell activation was inhibited,the expression of PPARγand IκBαwas significantly higher,and the expression of NF-κB was significantly lower in the treatment group as compared with the model group.Conclusions:ALHXW treatment can alleviate CCl4-induced liver fibrosis in rats, and the potential antifibrogenic mechanisms may occur through the upregulation of PPARγ expression and downregulation of NF-κB/IκBα signaling pathway.

关键词： Anluohuaxianwan,hepatic fibrosis,mechanism,nuclear factor-kappa B/IκBα, peroxisome proliferator-activated receptor-gamma

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The intrinsic PEDF is regulated by PPARγin permanent focal cerebral ischemia of rat

The intrinsic PEDF is regulated by PPARγin permanent focal ...

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2014中国医师协会中西医结合医师大会

作者：祝春华张祥建乔会敏王力娜张晓林河北医科大学第二医院神经内科

Background and object:Inflammatory damage plays a pivotal role in cerebral ischemia and may represent a target for treatment.Pigment epithelium-derived factor(PEDF) is proven to possess neuroprotective property.But there is little known about the intrinsic PEDF after cerebral ischemia.This study evaluated the time course expression of the intrinsic PEDF and its underlying regulation mechanisms after cerebral ischemia.Methods:Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion.Telmisartan(PPARy agonist) and GW9662(PPARy antagonist) were systemically administered to explore the effect on PPARy,PEDF,NF-kB and MMP-9 expression at 24 h after cerebral ischemia by western blot and qRT-PCR.The neurological deficits,brain water content and infarct volume were measured.Compared with normal group,the expressions of PEDF and PPARy decreased,and the expression of NF-kB and MMP-9 increased at early stage after ischemia(P < 0.05).Results;Compared with the vehicle group,the decrease of PEDF and PPARy was significantly up-regulated and the increase of NFkB and MMP-9 was down-regulated by telmisartan at 24 h(P < 0.05).The neurological deficits,brain water content and infarct volume were dramatically alleviated by telmisartan(P < 0.05).Telmisartan’s effects were reversed by GW9662 co-administration(P < 0.05).Conclusion;The expression of intrinsic PEDF was downregulated at the early stage of cerebral ischemia.The protective effects of intrinsic PEDF by activating PPARy pathway may be one of the strategic targets for cerebral ischemic therapies.

关键词： Peroxisome proliferator-activated receptor-gamma Pigment epithelium-derived factor Matrix metalloproteinases-9 Nuclear factor-KB Cerebral ischemia Telmisartan

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