1. Cortex Dictamni extract induces apoptosis of activated hepatic stellate cells via STAT1 and attenuates liver fibrosis in mice
- Author
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Wu, Xing-Xin, Wu, Li-Mei, Fan, Jing-Jing, Qin, Yu, Chen, Gong, Wu, Xue-Feng, Shen, Yan, Sun, Yang, and Xu, Qiang
- Subjects
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LIVER disease prevention , *FIBROSIS , *ALTERNATIVE medicine , *ANALYSIS of variance , *ANIMAL experimentation , *APOPTOSIS , *BIOLOGICAL assay , *BIOPHYSICS , *COLLAGEN , *HIGH performance liquid chromatography , *HISTOLOGICAL techniques , *RESEARCH methodology , *MEDICINAL plants , *BOTANIC medicine , *CHINESE medicine , *MICE , *RESEARCH funding , *STAINS & staining (Microscopy) , *STATISTICS , *T-test (Statistics) , *WESTERN immunoblotting , *DATA analysis , *PREVENTION - Abstract
Abstract: Ethnopharmacological relevance: In traditional Chinese medicines, Cortex Dictamni is prescribed for the treatment of a variety of inflammatory diseases such as acute rheumatoid arthritis, skin inflammation and jaundice. Aim of the study: This study was designed to investigate the effect of ethanol extract of Cortex Dictamni on treatment of hepatic fibrosis and its possible mechanisms. Materials and methods: The in vivo effect of Cortex Dictamni extract (CDE) was evaluated by measuring histological changes and collagen content in CCl4-indcued hepatic fibrosis mice. Viability, apoptosis and protein expression of hepatic stellate cells (HSC) were analyzed by MTT, Annexin V staining and Western blot respectively. Results: CDE alleviated CCl4-induced hepatic fibrosis in mice and showed a much stronger inhibition of cell viability in activated HSC cell line HSC-T6 than that in normal hepatocyte L02 cells. Furthermore, CDE induced apoptosis of HSC-T6 cells associated with increased expressions of cleaved PARP and cleaved caspase-3. Interestingly, CDE activated STAT1 in HSC-T6 cells and the effect of CDE on apoptosis of HSC-T6 cells could be neutralized using JAK/STAT1 signaling inhibitor AG490. Conclusions: These findings suggest that CDE possesses anti-fibrosis activity with selectively induction of activated HSC apoptosis via activating STAT1, which might be a novel strategy for hepatic fibrosis therapy. [Copyright &y& Elsevier]
- Published
- 2011
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