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Effects of exogenous thymosin ?4 on carbon tetrachloride-induced liver injury and fibrosis.

ABSTRACT: The present study investigated the effects of exogenous thymosin ?4 (TB4) on carbon tetrachloride (CCl₄)-induced acute liver injury and fibrosis in rodent animals. Results showed that both in mice and rats CCl₄ rendered significant increases in serum alanine aminotransferase and aspartate aminotransferase, hepatic malondialdehyde formation, decreases in antioxidants including superoxide dismutase and glutathione, and up-regulated expressions of transforming growth factor-?1, ?-smooth muscle actin, tumor necrosis factor-? and interleukin-1? in the liver tissues. Hydroxyproline contents in the rat livers were increased by CCl₄. Histopathological examinations indicated that CCl₄ induced extensive necrosis in mice livers and pseudo-lobule formations, collagen deposition in rats livers. However, all these changes in mice and rats were significantly attenuated by exogenous TB4 treatment. Furthermore, up-regulations of nuclear factor-?B p65 protein expression by CCl₄ treatment in mice and rats livers were also remarkably reduced by exogenous TB4 administration. Taken together, findings in this study suggested that exogenous TB4 might prevent CCl₄-induced acute liver injury and subsequent fibrosis through alleviating oxidative stress and inflammation.

SUBMITTER: Li X

PROVIDER: S-EPMC5517632 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Effects of exogenous thymosin β4 on carbon tetrachloride-induced liver injury and fibrosis.

Li Xiankui X Wang Lei L Chen Cai C

Scientific reports 20170719 1

The present study investigated the effects of exogenous thymosin β4 (TB4) on carbon tetrachloride (CCl<sub>4</sub>)-induced acute liver injury and fibrosis in rodent animals. Results showed that both in mice and rats CCl<sub>4</sub> rendered significant increases in serum alanine aminotransferase and aspartate aminotransferase, hepatic malondialdehyde formation, decreases in antioxidants including superoxide dismutase and glutathione, and up-regulated expressions of transforming growth factor-β1 ...[more]

PMID: 28724974

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Project description:Background: Liver fibrosis is a complex inflammatory and fibrogenic process, and the progression of fibrosis leads to cirrhosis. The only therapeutic approaches are the removal of injurious stimuli and liver transplantation. Therefore, the development of anti-fibrotic therapies is desired. Palmitoylethanolamide (PEA) is an endogenous fatty acid amide belonging to the N-acylethanolamines family and contained in foods such as egg yolks and peanuts. PEA has therapeutic anti-inflammatory, analgesic, and neuroprotective effects. However, the effects and roles of PEA in liver fibrosis remain unknown. Here we investigated the therapeutic effects of PEA in rats with liver fibrosis. Methods: We conducted in vitro experiments to investigate the effects of PEA on the activation of hepatic stellate cells (HSCs, LX-2). Liver fibrosis was induced by an intraperitoneal injection of 1.5 mL/kg of 50% carbon tetrachloride twice a week for 4 weeks. Beginning at 3 weeks, PEA (20 mg/kg) was intraperitoneally injected thrice a week for 2 weeks. Then rats were sacrificed and we performed histological and quantitative reverse-transcription polymerase chain reaction analyses. Results: The expression of α-smooth muscle actin (SMA) induced by transforming growth factor (TGF)-β1 in HSCs was significantly downregulated by PEA. PEA treatment inhibited the TGF-β1-induced phosphorylation of SMAD2 in a dose-dependent manner, and upregulated the expression of SMAD7. The reporter gene assay demonstrated that PEA downregulated the transcriptional activity of the SMAD complex upregulated by TGF-β1. Administration of PEA significantly reduced the fibrotic area, deposition of type I collagen, and activation of HSCs and Kupffer cells in rats with liver fibrosis. Conclusion: Activation of HSCs was significantly decreased by PEA through suppression of the TGF-β1/SMAD signaling pathway. Administration of PEA produced significant improvement in a rat model of liver fibrosis, possibly by inhibiting the activation of HSCs and Kupffer cells. PEA may be a potential new treatment for liver fibrosis.

Dataset Information

Effects of exogenous thymosin ?4 on carbon tetrachloride-induced liver injury and fibrosis.

Publications

Effects of exogenous thymosin β4 on carbon tetrachloride-induced liver injury and fibrosis.

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