Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

authored by

Marawan A Elbaset, Bassim M S A Mohamed, Shaimaa A Gad, Sherif M Afifi, Tuba Esatbeyoglu, Sahar S Abdelrahman, Hany M Fayed

Abstract

The kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis.

Organisation(s)

Institute of Food Science and Human Nutrition
Molecular Food Chemistry and Food Development

External Organisation(s)

Medical Research and Clinical Studies Institute
University of Sadat City
Cairo University

Type

Article

Journal

Scientific Reports

Volume

13

ISSN

2045-2322

Publication date

11.09.2023

Publication status

Published

Peer reviewed

Yes

ASJC Scopus subject areas

General

Electronic version(s)

https://doi.org/10.1038/s41598-023-42210-1 (Access: Open)