Effect of thymosin β4 on a mouse model of carbon tetrachloride-induced hepatic fibrosis and its mechanism
- VernacularTitle:胸腺素β4对四氯化碳诱导的肝纤维化小鼠模型的影响及其作用机制
- Author:
Yunhan ZHU
1
;
Siqi WANG
2
;
Dengya JING
2
;
Qinying FENG
3
Author Information
- Publication Type:Journal Article
- Keywords: Hepatic Fibrosis; Thymosin Beta 4; Mice， Inbred C57BL
- From: Journal of Clinical Hepatology 2026;42(3):593-599
- CountryChina
- Language:Chinese
- Abstract: ObjectiveTo 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. MethodsA 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. ResultsCompared 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. ConclusionTβ4 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.
