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Updated: Mar 3, 2026

The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Notch signaling mediated by TGF-β/Smad pathway in concanavalin A-induced liver fibrosis in rats
Yi Wang1, Ruo-Wu Shen1, Bing Han1
1Yi Wang, Zhen Li, Le Xiong, Feng-Yu Zhang, Bei-Bei Cong, Bei Zhang, Department of Immunology, Medical College of Qingdao University, Qingdao 266071, Shandong Province, China.
Aim:
To explore the exact interaction between Notch and transforming growth factor (TGF)-β signaling in liver fibrosis.
Methods:
We established a rat model of liver fibrosis induced by concanavalin A. Peripheral blood mononuclear cells (PBMCs) were isolated from the modeled rats, and cultured with γ-secretase inhibitor DAPT and TGF-β inhibitor for 24 h. The mRNA levels of Notch and TGF-β signaling were detected by quantitative real-time polymerase chain reaction. Expression of Notch and TGF-β proteins was analyzed by western blotting.
Results:
Compared to control rats, Notch and TGF-β signaling was activated in PBMCs of model rats. Administration of DAPT and TGF-β inhibitor suppressed Notch and TGF-β signal transducer in PBMCs of model rats. DAPT reduced mRNA and protein expression of TGF-β signaling, such as TGF-β1 and Smad3. TGF-β inhibitor also downregulated Notch1, Hes1 and Hes5, and mRNA and protein expression of the Notch signaling pathway.
Conclusion:
Notch and TGF-β signaling play a role in liver fibrosis. TGF-β signaling upregulates Notch signaling, which promotes TGF-β signaling.
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