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

verfasst von

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.

Organisationseinheit(en)

Institut für Lebensmittelwissenschaft und Humanernährung
Molekulare Lebensmittelchemie und -entwicklung

Externe Organisation(en)

Clinical Research Center Cairo (CRC)
University of Sadat City
Cairo University

Typ

Artikel

Journal

Scientific Reports

Band

13

ISSN

2045-2322

Publikationsdatum

11.09.2023

Publikationsstatus

Veröffentlicht

Peer-reviewed

Ja

ASJC Scopus Sachgebiete

Allgemein

Elektronische Version(en)

https://doi.org/10.1038/s41598-023-42210-1 (Zugang: Offen)