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CN 22-1108/R
Volume 42 Issue 3
Mar.  2026
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Article Navigation >  Journal of Clinical Hepatology  > 2026  >  42(3): 593-599

Effect of thymosin β4 on a mouse model of carbon tetrachloride-induced hepatic fibrosis and its mechanism

DOI: 10.12449/JCH260314
  • 1.

    Department of General Surgery，The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine，Guiyang 550000，China

  • 2.

    First Department of Blood Donation Service，Guizhou Blood Center，Guiyang 550000，China

  • 3.

    Central Laboratory，Guizhou Hospital，Beijing Jishuitan Hospital，Guiyang 550014，China

Research funding:

Guizhou Provincial Science and Technology Program Project (Qiankehe Chengguo-LC［2024］002);

Guizhou Provincial Health Commission Science and Technology Fund Project (gzwkj2026-619);

Beijing Jishuitan Hospital Guizhou Branch Hospital-level Research Fund Project (JGYYK［2025］09)

More Information
  • Corresponding author: FENG Qinying， 57105762@qq.com （ORCID： 0000-0001-6635-7086）
  • Received Date: 2025-08-19
  • Accepted Date: 2025-11-06
  • Published Date: 2026-03-25
    Abstract
  •   Objective  To investigate the therapeutic effect and potential mechanism of thymosin β4 （Tβ4） on carbon tetrachloride （CCl4）-induced hepatic fibrosis by regulating the expression of platelet-derived growth factor （PDGF） and inducing the apoptosis of hepatic stellate cell （HSC）， and to provide new experimental evidence for anti-hepatic fibrosis treatment in clinical practice.  Methods  A total of 30 male C57 mice were randomly divided into normal control group， model group， low-dose Tβ4 treatment group （3 mg/kg）， middle-dose Tβ4 treatment group （6 mg/kg）， and high-dose Tβ4 treatment group （12 mg/kg）， with 6 mice in each group. The mice in the normal control group were fed with a normal diet ad libitum， and those in the other groups were given intraperitoneal injection of 50% CCl4 mixed with olive oil to establish a model of hepatic fibrosis. After successful modeling confirmed by ultrasound and histopathology， the mice in each treatment group were given subcutaneous injection of Tβ4 for 4 consecutive weeks. Liver tissue was collected at the end of the experiment， and HE staining and Masson staining were used to observe histopathological changes； quantitative real-time PCR was used to measure the mRNA expression level of PDGF； TUNEL assay was used to assess the apoptosis of HSC. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups.  Results  Compared with the model group， the middle- and high-dose Tβ4 treatment groups had varying degrees of alleviation of hepatic fibrosis. Quantitative real-time PCR showed that Tβ4 could significantly downregulate the mRNA expression level of PDGF in liver tissue， with a significant difference between the treatment groups （P>0.05）， and there was no significant difference in the mRNA expression level of PDGF between the high-dose Tβ4 treatment group and the normal control group （P>0.05）. TUNEL assay showed that the middle- and high-dose Tβ4 treatment groups had a significantly higher number of apoptotic HSCs than the model group.  Conclusion  Tβ4 may improve CCl4-induced hepatic fibrosis in mice by downregulating the expression of PDGF and promoting the apoptosis of HSC， suggesting that it has a potential application value in the treatment of hepatic fibrosis.

     

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