Details
| Original language | English |
|---|---|
| Article number | 14929 |
| Journal | Scientific Reports |
| Volume | 13 |
| Issue number | 1 |
| Publication status | Published - 11 Sept 2023 |
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.
Keywords
- Animals, Rats, AMP-Activated Protein Kinases, Thioacetamide/toxicity, STAT5 Transcription Factor, Erythropoietin/pharmacology, Kidney
ASJC Scopus subject areas
Cite this
- Standard
- Harvard
- Apa
- Vancouver
- BibTeX
- RIS
In: Scientific Reports, Vol. 13, No. 1, 14929, 11.09.2023.
Research output: Contribution to journal › Article › Research › peer review
}
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 -