Insights into the impact of fxr activation on hepatic autophagy in a non-alcoholic steatohepatitis model

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Tawfiq R.A.; Attia Y.M.; Nassar N.N.; Hammam O.A.; Elmazar M.M.; Abdallah D.M.

Journal: Bulletin of Pharmaceutical Sciences. Assiut

Publisher: Assiut University

Publication Date: 1 June 2021

Volume / Issue: Volume 44 / Issue 1

Pages: 265–274

ISSN: 11100052

DOI: 10.21608/BFSA.2021.174153

Scopus: View on Scopus

Document Type: Article

Access: All Open Access; Gold Open Access; Green Open Access

Authors and Affiliations

Tawfiq R.A., Department of Pharmacology, Faculty of Pharmacy, British University in Egypt, Cairo, Egypt; Attia Y.M., Department of Pharmacology, Faculty of Pharmacy, British University in Egypt, Cairo, Egypt; Nassar N.N., Department of Pharmacology, Faculty of Pharmacy, Cairo University, Cairo, Egypt; Hammam O.A., Department of Pathology, Theodor Bilharz Research Institute, Cairo, Egypt; Elmazar M.M., Department of Pharmacology, Faculty of Pharmacy, British University in Egypt, Cairo, Egypt; Abdallah D.M., Department of Pharmacology, Faculty of Pharmacy, Cairo University, Cairo, Egypt

Abstract

Background: Multiple lines of evidence pointed to the role of dysbiosis, small intestinal bacterial overgrowth and altered intestinal permeability in promoting pro-inflammatory events in the liver leading to the progression of steatosis to non-alcoholic steatohepatitis (NASH). The pivotal involvement of farnesoid-X-receptor (FXR) in maintaining intestinal homeostasis and combating hepatic inflammation was previously established. Nonetheless, the role of hepatic autophagy in NASH pathogenesis and treatment remains controversial. The present study aimed at investigating whether the effect of the FXR agonist, obeticholic acid, on ameliorating NASH-related incidents is related to an impact on hepatic autophagy. Methods: Swiss albino mice were fed an atherogenic high fat diet (Ath-HFD) with dextran sulfate sodium (DSS) in drinking water to induce NASH. Obeticholic acid (5 mg/kg/day, p.o.) was given for 28 days, starting at day 64 post NASH initiation. Histopathological examination of liver and colon samples was performed. Inflammatory markers, IL-1β, IL-6, IFN-γ and TNF-α, besides adiponectin, were assessed in the liver. Autophagy genes, ULK1, BECN-1 and ATG5, were assessed by RT-PCR in hepatic tissues. Results: Histopathological changes observed in the liver and colon of the positive control group (Ath-HFD/DSS) were significantly ameliorated after treatment. No noticeable changes were reported in adiponectin and inflammatory markers following treatment except for a partial enhancement in IFN-γ. Though ULK1 and BECN-1 gene expression tended to increase after treatment with obeticholic acid compared to Ath-HFD/DSS group, ATG5 mRNA was almost restored. Conclusion: Obeticholic acid ameliorated NASH partially through autophagy and IFN-γ enhancements in the liver. © 2021 Assiut University. All rights reserved.

Keywords

adiponectin; autophagy related protein 5; beclin 1; dextran sulfate; farnesoid X receptor; gamma interferon; interleukin 1beta; interleukin 6; messenger RNA; obeticholic acid; serine threonine protein kinase ULK1; tumor necrosis factor; animal cell; animal experiment; animal model; animal tissue; Article; autophagy (cellular); colon; controlled study; enzyme linked immunosorbent assay; gene expression; histopathology; lipid diet; liver tissue; male; mouse; nonalcoholic steatohepatitis; nonhuman; protein expression; protein function; real time polymerase chain reaction; transcription initiation

Citation Information

Scopus Citations: 1

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