IUBMB life, 2018-06, Vol.70 (6), p.511-518
2018
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- Autor(en) / Beteiligte
- Titel
- Effect of histone deacetylase inhibitor on epithelial‐mesenchymal transition of liver fibrosis
- Ist Teil von
- IUBMB life, 2018-06, Vol.70 (6), p.511-518
- Ort / Verlag
- England: Wiley Subscription Services, Inc
- Erscheinungsjahr
- 2018
- Quelle
- Wiley Online Library Journals【Remote access available】
- Beschreibungen/Notizen
- Liver fibrosis is an excessively reversible wound healing process and the fibrotic disorder is the activation of hepatic stellate cell that requires extensive alterations in gene expression. As reversible deacetylation of histone proteins modulate gene expression, we examined the effect of valproic acid (VPA) as selective histone deacetylase inhibitor on CCl‐4 induced liver fibrosis. Thirty rats were divided into three equal groups; control group, fibrotic group and VPA‐treated group. The rats were sacrificed after 6 weeks of liver fibrosis induction. The histopathological effect on liver tissue was examined. The expression of α‐SMA and Smad‐4 mRNA and serum levels of TGF‐β1, alanine aminotransferase, and aspartate aminotransferase were determined. Treatment of rats with VPA attenuated carbon tetrachloride‐induced liver fibrosis. Moreover, α‐SMA and Smad‐4 expression was repressed under VPA treatment and both serum TGF‐β1 and liver enzymes were significantly decreased. The histone deacetylase inhibitor‐1 VPA inhibits the epithelial–mesenchymal transition and affects hepatic stellate cell activation during liver fibrosis through downregulation of Smad4 and α‐SMA expression which may serve as a promising agent in liver fibrosis treatment. © 2018 IUBMB Life, 70(6):511–518, 2018
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1521-6543eISSN: 1521-6551DOI: 10.1002/iub.1742Titel-ID: cdi_proquest_miscellaneous_2020489248
- Format
- –
- Schlagworte
- Alanine, Alanine transaminase, and Smad‐4, Animals, Aspartate aminotransferase, Bile, Carbon tetrachloride, Carbon Tetrachloride - toxicity, Cell activation, Cells, Cultured, Chromatin, Deacetylation, Epithelial-Mesenchymal Transition - drug effects, Fibrosis, Gene expression, Hepatic Stellate Cells - drug effects, Hepatic Stellate Cells - metabolism, Hepatic Stellate Cells - pathology, Hepatocytes, Histone deacetylase, histone deacetylase inhibitor, Histone Deacetylase Inhibitors - pharmacology, Liver, Liver Cirrhosis - chemically induced, Liver Cirrhosis - drug therapy, Liver Cirrhosis - metabolism, Liver Cirrhosis - pathology, liver fibrosis, Male, Mesenchyme, Rats, Rats, Wistar, Serum levels, Signal Transduction, Smad protein, Smad4 protein, TGF‐β, Transforming growth factor-b1, Valproic acid, Wound healing, α‐SMA