Therapeutic Impact of Telmisartan Against The Thioacetamide Induced Hepatic Fibrosis In Rats

Document Type : Research and Reference

Authors

1 Chemistry department (Biochemistry Division)-Faculty of Science-ElMinia University-ElMinia-Egypt

2 Chemistry Department, Faculty of Science ElMinia University, 61519 El-Minya, Egypt

3 Professor of Biochemistry, Department of Biochemistry, Faculty of Medicine, Minia University, Dean of Faculty of Pharmacy, Deraya University

4 Prof of histology Histology department, Faculty of Medicine, Minia University

10.21608/djs.2024.321762.1189

Abstract

Background: Hepatic fibrosis is a severe condition related to ongoing liver disorders. Liver fibrosis evolves in response to multiple causes of chronic hepatic disease. At present, the mechanism of its occurrence has yet to be determined, and there are no viable therapeutic medicines. Goal: Our aim was to determine the potential of Telmisartan to inhibit the progression of hepatic fibrosis induced in albino rats. Material and methods: In a recent study, Thioacetamide was used to induce hepatic fibrosis in a rat model. Randomly, forty albino rats were classified into four identical groups (ten rats per group). These groups were Healthy group, fibrotic group, Prophylactic group with Telmisartan and treated group with Telmisartan. Biochemical and histological analysis were evaluated. By using ELISA, IL-6, IL-1B, and TNF-α were examined. Results: The results revealed that there was very highly significant decreased (P<0.0001) in ALT, ALP, AST, Total Bilirubin and Direct Bilirubin levels in groups which treated with Telmisartan (G3, G4) compared with fibrotic group (G2), while there was highly significant increase in albumin (p<0.001) in Telmisartan treated group. Liver sections from talmisartan groups showed markedly decreased hepatic lesions. We found a very highly significant effect of Telmisartan on IL-6, IL-1B, and TNF-α levels. Conclusion: There are a potential therapeutic value and antifibrotic effects of Telmisrtan on hepatic fibrosis in the thioacetamide model.

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