Related Experiment Video
Updated: Mar 22, 2026
A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia
Published on: February 3, 2023
[Experimental study on effect of model on hepatic fibrosis with Aralia chinesis]
Abstract:
Hepatic fibrosis models were induced by CCl4 in rats. To explore vascular endothelial growth factor (VEGF), transforming growth factor-beta1 (TGFβ1) mRNA expression and bcl-2, Bax protein expression levels of intervention and explore the mechanism of the Aralia chinesis anti-hepatic fibrosis. Sixty male Sprague-Dawlley (SD) rats were randomly divided into six groups: nomal group, model group, high-dose (10 mL x kg(-1)), medium-dose (7.5 mL x kg(-1)), low-dose (5.0 mL x kg(-1)) of A. chinesis treated group and colchicine treated group. The change of liver histopathology was observed by HE and Masson staining. The mRNA of VEGF, TGF-β1 were detected by RT-PCR. The protein of Bcl-2 and Bax were detected by Western blot. In the model group liver cell obvious degeneration, necrosis, a large number of collagen fibers of the cable hyperplasia, part visible pseudolobule formation. A. chinesis large, medium, low-dose group and colchicine group liver cell degeneration and necrosis reduced A. chinesis small, medium, and high-dose group was gradually reduced trend and A. chinesis large, middle dose group degree of reduction is particularly significant. Compared with model group, A. chinesis of large, medium and small dose group and colchicine group VEGF mRNA expression, A. chinesis of large, medium-dose group TGF-β1 mRNA expression reduce (P < 0.05); compared with colchicine group, A. chinesis of large, middle dose group of VEGF mRNA expression decreased (P < 0.05); A. chinesis of large, middle dose group of TGF-β1 mRNA expression decreased (P < 0.01), and compared with colchicine group, large dose group of of TGF-β1 mRNA expression decreased (P < 0.05). Compared with model group, A. chinesis of large, medium and small dose group and colchicine group Bcl-2 protein expression reduce (all is P < 0.05). But A. chinesis of large, medium and small dose group and colchicine group of Bax protein expression were increased (P < 0.05). A. chinesis regulation of VEGF, TGF-β1 may prevent the activation of hepatic stellate cells, liver tissue by up regulating the anti-apoptotic protein Bax and down pro-apoptotic protein Bcl-2 expression, thereby to improve the degree of liver fibrosis.
Insights
Aralia chinesis extract effectively reduced liver fibrosis in rats by modulating key molecular markers. This study highlights its potential as a therapeutic agent for hepatic fibrosis.
Area of Science:
- Pharmacology
- Hepatology
- Molecular Biology
Context:
- Carbon tetrachloride (CCl4) is a common inducer of experimental hepatic fibrosis.
- Hepatic fibrosis is characterized by excessive extracellular matrix deposition, leading to liver damage.
- Understanding the molecular mechanisms underlying fibrosis is crucial for developing effective treatments.
Purpose:
- To investigate the anti-fibrotic effects of Aralia chinesis extract in a rat model.
- To explore the impact of Aralia chinesis on the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-β1) mRNA.
- To analyze the protein expression levels of Bcl-2 and Bax in response to Aralia chinesis treatment.
Summary:
- CCl4-induced hepatic fibrosis in rats was treated with varying doses of Aralia chinesis extract and colchicine.
- Histopathological examination revealed reduced liver cell degeneration and necrosis in treated groups.
- Aralia chinesis significantly downregulated VEGF and TGF-β1 mRNA expression and modulated Bcl-2 and Bax protein levels, indicating an anti-apoptotic and anti-fibrotic effect.
Impact:
- Aralia chinesis demonstrates potential therapeutic value in mitigating liver fibrosis.
- The study elucidates the molecular pathways through which Aralia chinesis exerts its protective effects.
- These findings may pave the way for novel therapeutic strategies targeting hepatic fibrosis.
