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Xiaochaihutang attenuates liver fibrosis by activation of Nrf2 pathway in rats.

Authors: Li, Jin  Hu, Rui  Xu, Shangfu  Li, Yuanyang  Qin, Ying  Wu, Qin  Xiao, Zhi 
Citation: Li J, etal., Biomed Pharmacother. 2017 Oct 18;96:847-853. doi: 10.1016/j.biopha.2017.10.065.
Pubmed: (View Article at PubMed) PMID:29078262
DOI: Full-text: DOI:10.1016/j.biopha.2017.10.065

Xiaochaihutang (XCHT) is a decoction of seven botanical extracts used for liver diseases traditionally in East Asia. However, few studies have investigated its anti-hepatic fibrosis effects and the mechanisms of action. Oxidative stress is one of the key factors responsible for occurrence and development of hepatic fibrosis and nuclear factor erythroid 2-related factor 2 (Nrf2) serves as a major regulator of the cellular defense system against oxidative stress. The aim of the present study was to investigate the effect of XCHT on liver fibrosis and focuse on the Nrf2 pathway in the protection of XCHT against CCl4-induced oxidative stress. Liver fibrosis was induced by repeated injection of CCl4 over a period of 9 weeks. Starting from the 6th week, rats in treatment groups were given the appropriate doses of XCHT granules and Silybin. We discovered that CCl4 caused significant fibrosis damage in rat liver, and XCHT (5g/kg and 10g/kg, po for 4 weeks) significantly improved the liver functions and fibrosis degree. XCHT treatment significantly decreased the number of α-SMA positive stained cells, indicating suppression of activated hepatic stellate cells (HSCs). Compared with the CCl4 treatment, administration of XCHT significantly increased the hepatic levels of Nqo1, HO-1, GCLC and GCLM, the major components of the Nrf2 pathway. These studies demonstrated that XCHT is an effective therapeutic agent for treatment of hepatic fibrosis and the mechanism of action might be due to up-regulation of the Nrf2 pathway against oxidative stress, making further inhibition of activated HSCs.

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RGD ID: 13442479
Created: 2017-11-02
Species: All species
Last Modified: 2017-11-02
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.