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other·preclinical research, gastroenterology, immunology, biomedical research·PMC10465256

Erythropoietin Suppresses the Hepatic Fibrosis Caused by Thioacetamide: Role of the PI3K/Akt and TLR4 Signaling Pathways

Oxidative Medicine and Cellular Longevity · 8 authors, 5 centres

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TL;DR

In male Wistar rats, erythropoietin (EPO) dose-dependently attenuated thioacetamide-induced liver fibrosis, as evidenced by reduced fibrosis, improved liver enzymes, and restored antioxidant levels. EPO's hepatoprotective effects were associated with upregulation of the PI3K/Akt survival pathway and downregulation of the TLR4 proinflammatory axis.

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EPO attenuated hepatic fibrosis dose-dependently, demonstrated by decreased serum ALT and AST, increased albumin, reduced tissue TNF-α, IL-1β, TGF-β1, and TLR4 levels, and elevated PI3K and p-PI3K levels. EPO restored hepatic glutathione and superoxide dismutase and prevented malondialdehyde accumulation. Immunohistochemistry confirmed decreased TLR4 protein expression, increased PI3K and Akt protein expression, and downregulated MAPK expression, with improved histological architecture. These findings suggest EPO may prevent TAA-induced hepatic fibrosis via PI3K/Akt upregulation and TLR4 downstream axis downregulation.

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preclinical research

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ORIGINAL PAPER

PMC10465256

Erythropoietin Suppresses the Hepatic Fibrosis Caused by Thioacetamide: Role of the PI3K/Akt and TLR4 Signaling Pathways

Oxidative Medicine and Cellular Longevity

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ABSTRACT

Abstract Erythropoietin (EPO) is recognized for its function in erythropoiesis; however, its potential antifibrotic effect against liver fibrosis remains unknown. This study examined whether EPO affects thioacetamide (TAA)-induced liver fibrosis by concentrating on the Toll-like receptor 4 (TLR4) cascade and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway as possible pathways. Male Wistar rats were randomized into four groups, which included: the negative control group, the TAA group (intraperitoneal; TAA 100 mg/kg three times per week for 2 weeks), and EPO-treated groups (150 and 300 IU/kg, i.p.) for 2 weeks after TAA injections. EPO attenuated hepatic fibrosis in a dosage-dependent way, as manifested by the diminution in serum alanine aminotransferase and aspartate aminotransferase activities, as well as the increase in albumin level. EPO inhibited the increase in tissue levels of tumor necrosis factors- α , interleukin-1 β , transforming growth factor- β 1, and TLR4 and raised tissue levels of PI3K and p -PI3K. EPO antioxidant properties were demonstrated by restoring hepatic glutathione and superoxide dismutase by preventing the accumulation of hepatic malondialdehyde. Further, EPO increased the protein expression of PI3K and Akt and decreased TLR4 protein expression. Immunohistochemically, EPO treatment altered tissue histology and downregulated mitogen-activated protein kinase protein expression. Overall, the research suggested that EPO could prevent TAA-induced hepatic fibrosis through upregulating the PI3K/Akt signaling cascade and downregulation the TLR4 downstream axis.

CITATION EXPORT

Marawan A Elbaset, Bassim M S A Mohamed, Passant E Moustafa et al.. Erythropoietin Suppresses the Hepatic Fibrosis Caused by Thioacetamide: Role of the PI3K/Akt and TLR4 Signaling Pathways. Oxidative Medicine and Cellular Longevity. (2023). https://doi.org/10.1155/2023/5514248

AUTHORS

8 · 5 CENTRES

Marawan A Elbaset, Bassim M S A Mohamed, Passant E Moustafa, Dina F Mansour, Sherif M Afifi, Tuba Esatbeyoglu, Sahar S M Abdelrahman, Hany M Fayed

1Pharmacology Department, Medical Research and Clinical Studies Institute, National Research Centre, 33 El-Bohouth St., Dokki, P.O. Box 12622, Cairo, Egypt
2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Galala University, Attaka, Suez, Egypt
3Pharmacognosy Department, Faculty of Pharmacy, University of Sadat City, Sadat City 32897, Egypt
4Department of Food Development and Food Quality, Institute of Food Science and Human Nutrition, Gottfried Wilhelm Leibniz University Hannover, Am Kleinen Felde 30, Hannover 30167, Germany
5Department of Pathology, College of Veterinary Medicine, Cairo University, P.O. Box 12211, Cairo, Egypt