Apigenin role against thioacetamide-triggered liver fibrosis: Deciphering the PPARγ/TGF-β۱/NF-κB and the HIF/FAK/AKT pathways
Publish place: Journal of Herbmed Pharmacology، Vol: 12، Issue: 2
Publish Year: 1401
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:
JR_HERM-12-2_004
تاریخ نمایه سازی: 14 آذر 1402
Abstract:
Introduction: Liver tissue malfunction is a severe worldwide health concern that arises from various chronic liver conditions. The goal of this investigation was to look into the anti-fibrotic effect of apigenin (APG), an antioxidant found in various plants, versus thioacetamide (TAA)-triggered hepatic scarring in rats and the potential mechanisms behind it.
Methods: TAA was administered thrice weekly (۱۰۰ mg/kg, i.p.) for two weeks to produce hepatic scarring. APG was administered after TAA for ۱۴ days (۵ or ۱۰ mg/kg, orally). Thereafter, hepatic liver enzymes, inflammatory markers, fibrotic indicators, and histopathological changes were evaluated.
Results: TAA increased the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), reduced albumin and total protein, elevated hepatic level of lipid peroxidation, focal adhesion kinase (FAK), hypoxia-inducible factor-۱α (HIF-۱α), and inflammatory cytokines, decreased interleukin-۱۰ (IL-۱۰), reduced hepatic expression of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor-erythroid factor ۲-related factor ۲ (Nrf۲), and elevated serine-threonine protein kinase (AKT) expression. Furthermore, TAA increased hepatic contents of collagen I, connective tissue growth factor (CTGF), hydroxyproline, and alpha-smooth muscle actin. On the other hand, APG evaded these changes and mitigated the harmful effects of TAA in a dose-dependent way. Histopathological and immunohistochemical observations reinforced these biochemical outcomes.
Conclusion: APG can potentially alleviate liver fibrosis mediated via FAK and HIF۱ inhibiting signaling pathways.
Keywords:
Malondialdehyde , Transforming growth factor beta ۱ , Tumour necrosis factor alpha Alpha-smooth muscle actin , Hydroxyproline , Liver fibrosis , Rats
Authors
Rehab F Abdel-Rahman
Department of Pharmacology, Medical Research and Clinical studies Institute, National Research Centre, Dokki, Giza ۱۲۶۲۲, Egypt
Hany M Fayed
Department of Pharmacology, Medical Research and Clinical studies Institute, National Research Centre, Dokki, Giza ۱۲۶۲۲, Egypt
Marwan Abd Elbaset Mohamed
Department of Pharmacology, Medical Research and Clinical studies Institute, National Research Centre, Dokki, Giza ۱۲۶۲۲, Egypt
Alyaa F Hessin
Department of Pharmacology, Medical Research and Clinical studies Institute, National Research Centre, Dokki, Giza ۱۲۶۲۲, Egypt