Article · Volume 22, Issue 4 · pp. 1617–1626
Rosiridin Attenuates Liver Injury by Modulating Antioxidant Activity and Inflammatory Markers in Thioacetamide-induced Liver Cirrhosis in Experimental Rats
Ying Chang1, Quanwei Di2, Shining Lou3, Jie Meng1, Xinli Feng4, Xinwen Zhang5
- 1Department of Gastroenterology, Affiliated Hospital of Hebei University, Baoding, Hebei, China.
- 2Department of Internal Medicine, Worker’s Hospital of China Lucky Group Cooperation, Baoding, Hebai, China.
- 3Department of Traditional Chinese Medicine, Worker’s Hospital of China Lucky Group Cooperation, Baoding, Hebai, China.
- 4Department of Emergency Medicine, Affiliated Hospital of Hebei University, Baoding, Hebei, China.
- 5Department of Integrated Traditional Chinese and Western Medicine, Affiliated Hospital of Hebei University, Baoding, Hebei, China.
Abstract
Background: Liver cirrhosis, a chronic and progressive liver disease, represents the end-stage of several hepatic injuries, characterized by widespread fibrosis, nodule formation, and ultimately, liver dysfunction and failure. Existing treatments often focus on managing complications rather than addressing the underlying pathological processes, which underscores the need for safer, potentially alternative therapeutic agents. Objectives: The present work was performed to assess the ameliorative mechanisms and hepatoprotective properties of rosiridin against thioacetamide-induced liver cirrhosis in experimental rats. Materials and Methods: Liver cirrhosis was experimentally induced in rats by administering 200 mg/kg of thioacetamide thrice per week for 2 months. Rosiridin and silymarin were administered to the rats for 2 months. After treatments, liver dysfunction markers and biochemical parameters were evaluated in the experimental rats. The concentrations of inflammatory and oxidative stress markers were evaluated in the experimental rats. The liver tissues were obtained and underwent histopathological assessments. Results: The present findings demonstrate that rosiridin treatment markedly reduced liver dysfunction markers and regulated serum biochemical markers in thioacetamide-induced rats. Furthermore, the treatment with rosiridin considerably reduced the pro-inflammatory cytokine levels and oxidative stress markers, while enhancing the antioxidant concentrations in the thioacetamide-induced rats. In addition, histopathological analysis revealed that rosiridin ameliorated histopathological alterations in thioacetamide-induced rats. Conclusion: The findings of this work indicated that rosiridin markedly ameliorated the development of thioacetamide-triggered liver cirrhosis in rats. These findings highlight that rosiridin may serve as a promising treatment agent for liver cirrhosis.
Keywords: Liver dysfunction; thioacetamide; rosiridin; liver cirrhosis; inflammation
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