TY - JOUR

T1 - Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway

AU - Elbaset, Marawan A

AU - Mohamed, Bassim M S A

AU - Gad, Shaimaa A

AU - Afifi, Sherif M

AU - Esatbeyoglu, Tuba

AU - Abdelrahman, Sahar S

AU - Fayed, Hany M

N1 - Publisher Copyright: © 2023, Springer Nature Limited.

PY - 2023/9/11

Y1 - 2023/9/11

N2 - 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.

AB - 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.

KW - Animals

KW - Rats

KW - AMP-Activated Protein Kinases

KW - Thioacetamide/toxicity

KW - STAT5 Transcription Factor

KW - Erythropoietin/pharmacology

KW - Kidney

UR - http://www.scopus.com/inward/record.url?scp=85170630863&partnerID=8YFLogxK

U2 - 10.1038/s41598-023-42210-1

DO - 10.1038/s41598-023-42210-1

M3 - Article

C2 - 37697015

VL - 13

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 14929

ER -