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J Herbmed Pharmacol. 2023;12(2): 202-213.
doi: 10.34172/jhp.2023.21

Scopus ID: 85158818382
  Abstract View: 1707
  PDF Download: 709

Original Article

Apigenin role against thioacetamide-triggered liver fibrosis: Deciphering the PPARγ/TGF-β1/NF-κB and the HIF/FAK/ AKT pathways

Rehab F. Abdel-Rahman 1* ORCID logo, Hany M. Fayed 1 ORCID logo, Marwan Abd Elbaset Mohamed 1 ORCID logo, Alyaa F. Hessin 1 ORCID logo, Gihan F. Asaad 1 ORCID logo, Sahar AbdelRahman 2 ORCID logo, Abeer A.A. Salama 1 ORCID logo, Mahmoud S. Arbid 1 ORCID logo, Hanan A. Ogaly 3 ORCID logo

1 Department of Pharmacology, Medical Research and Clinical studies Institute, National Research Centre, Dokki, Giza 12622, Egypt
2 Department of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt
3 Department of Biochemistry, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt
*Corresponding Author: Abdel-Rahman, Email: rehabs2001@yahoo. com, , Email: rf.abdelrahman@nrc.sci.eg

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 antifibrotic 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 (100 mg/kg, i.p.) for two weeks to produce hepatic scarring. APG was administered after TAA for 14 days (5 or 10 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-1α (HIF-1α), and inflammatory cytokines, decreased interleukin-10 (IL-10), reduced hepatic expression of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor-erythroid factor 2-related factor 2 (Nrf2), 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 HIF1 inhibiting signaling pathways.


Implication for health policy/practice/research/medical education:

Our research showed that apigenin has the potential to be a therapeutic medication for hepatic fibrosis. However, further studies are needed to establish the clinical applicability of APG treatment in active liver fibrogenesis human cases.

Please cite this paper as: Abdel-Rahman RF, Fayed HM, Mohamed MA, Hessin AF, Asaad GF, AbdelRahman S, et al. Apigenin role against thioacetamide-triggered liver fibrosis: Deciphering the PPARγ/TGF-β1/NF-κB and the HIF/FAK/AKT pathways. J Herbmed Pharmacol. 2023;12(2):202-213. doi: 10.34172/jhp.2023.21.

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Submitted: 02 Nov 2022
Revision: 23 Dec 2022
Accepted: 24 Dec 2022
ePublished: 18 Mar 2023
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