Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway
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...
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| Format: | Article |
| Language: | English |
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Nature Portfolio
2023-09-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-023-42210-1 |
| _version_ | 1797452667009630208 |
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| author | Marawan A. Elbaset Bassim M. S. A. Mohamed Shaimaa A. Gad Sherif M. Afifi Tuba Esatbeyoglu Sahar S. Abdelrahman Hany M. Fayed |
| author_facet | Marawan A. Elbaset Bassim M. S. A. Mohamed Shaimaa A. Gad Sherif M. Afifi Tuba Esatbeyoglu Sahar S. Abdelrahman Hany M. Fayed |
| author_sort | Marawan A. Elbaset |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-09T15:11:57Z |
| format | Article |
| id | doaj.art-9ec20c69b95d44a6804b9808b693bf6f |
| institution | Directory Open Access Journal |
| issn | 2045-2322 |
| language | English |
| last_indexed | 2024-03-09T15:11:57Z |
| publishDate | 2023-09-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Scientific Reports |
| spelling | doaj.art-9ec20c69b95d44a6804b9808b693bf6f2023-11-26T13:20:17ZengNature PortfolioScientific Reports2045-23222023-09-0113111210.1038/s41598-023-42210-1Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathwayMarawan A. Elbaset0Bassim M. S. A. Mohamed1Shaimaa A. Gad2Sherif M. Afifi3Tuba Esatbeyoglu4Sahar S. Abdelrahman5Hany M. Fayed6Pharmacology Department, Medical Research and Clinical Studies Institute, National Research CentrePharmacology Department, Medical Research and Clinical Studies Institute, National Research CentrePharmacology Department, Medical Research and Clinical Studies Institute, National Research CentrePharmacognosy Department, Faculty of Pharmacy, University of Sadat CityDepartment of Food Development and Food Quality, Institute of Food Science and Human Nutrition, Gottfried Wilhelm Leibniz University HannoverDepartment of Pathology, Faculty of Veterinary Medicine, Cairo UniversityPharmacology Department, Medical Research and Clinical Studies Institute, National Research CentreAbstract 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.https://doi.org/10.1038/s41598-023-42210-1 |
| spellingShingle | Marawan A. Elbaset Bassim M. S. A. Mohamed Shaimaa A. Gad Sherif M. Afifi Tuba Esatbeyoglu Sahar S. Abdelrahman Hany M. Fayed Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway Scientific Reports |
| title | Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway |
| title_full | Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway |
| title_fullStr | Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway |
| title_full_unstemmed | Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway |
| title_short | Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway |
| title_sort | erythropoietin mitigated thioacetamide induced renal injury via jak2 stat5 and ampk pathway |
| url | https://doi.org/10.1038/s41598-023-42210-1 |
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