Premium
Ursodesoxycholic acid Display a Role of Experimental Anti‐hepatic Fibrosis by Inhibiting the Expression of Bnip3L Protein
Author(s) -
Teng LinHua,
Liu QiLin,
Zhang JiWang,
Liu ZeFeng,
Chen Li,
Zhang Guo
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.840.2
Subject(s) - hepatic stellate cell , hepatic fibrosis , ccl4 , in vivo , messenger rna , fibrosis , western blot , chemistry , immunohistochemistry , pathology , cancer research , medicine , carbon tetrachloride , biology , biochemistry , gene , microbiology and biotechnology , organic chemistry
Backgound & Aims Previous reports showed that ursodesoxycholic acid (UDCA) might has an therapeutic effect on liver fibrosis, but the detail pharmacological mechanism remains unclear. This study was aimed to study the relationship between the expression change of mitochondrial Bnip3L protein and inhibitory role of UDCA for experimental hepatic fibrosis. Methods Hepatic stellate cell (HSC)‐LX2 cell line and CCl4‐induced hepatic fibrotic rats model were used in the in vitro or in vivo regimens with UDCA or vehicle control. Western Blot was then performed to analyze the expression of α‐SMA and Bnip3L in LX2 cells. Real‐time fluorescence quantitative PCR (qRT‐PCR) was performed to compare the differential expression of COL1 mRNA in LX2 cells and COL1 mRNA. Bnip3L mRNA in liver tissues among these different groups. The liver fibrosis of rats was evaluated by Masson staining. Results Our research showed that the expression of Bnip3L protein was significantly inhibited by UDCA in LX2 cells which were activated by TGF‐β1, and that was positively correlated with the down‐regulated expression of α‐SMA and COL1 mRNA. UDCA could significantly reduce the production of collagen in liver tissues of CCl4‐induced liver fibrosis. In parallel, the expression of Bnip3L mRNA and COL1 mRNA were simultaneously inhibited by UDCA in these liver tissues. Conclusions Our findings demonstrate that UDCA displays a critical role of anti‐hepatic fibrosis by down‐regulating the expression of Bnip3L protein, which may provide a novel pharmacological strategy for liver fibrosis in the future. Support or Funding Information Supported by NSFC Grants 81360077, 30630145, 81172260 and GXNSFC Grants 2015GXNSFDA139022 to Guo Zhang This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .