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ORIGINAL ARTICLE
Year : 2019  |  Volume : 5  |  Issue : 2  |  Page : 95-103

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


1 Department of Microbiology and Center of Infectious Diseases, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China
2 Department of Microbiology and Center of Infectious Diseases, Peking University Health Science Center, Beijing; Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
3 Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China

Correspondence Address:
Hui Zhuang
Department of Microbiology and Center of Infectious Diseases, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191
China
Xue-En Liu
Department of Microbiology and Center of Infectious Diseases, School of Basic Medical Sciences, Health Science Center, Peking University, Beijing 100191
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/wjtcm.wjtcm_16_19

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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 tetrachloride (CCl4)-induced liver fibrosis. Methods: Thirty-six male Wistar rats were randomly assigned into three groups: control, model, and treatment. The model and treatment groups were injected intraperitoneally with 40% CCl4(2 ml/kg), and the control group was given saline (2 ml/kg) twice a week for 6 weeks. In parallel, the treatment group was gavaged with ALHXW solution daily, while the control and 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 Inhibitor α of 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 PPARγ and IκBα was 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.


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