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. 2023 Sep 11;13(1):14929.
doi: 10.1038/s41598-023-42210-1.

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

Marawan A Elbaset  1 , Bassim M S A Mohamed  2 , Shaimaa A Gad  2 , Sherif M Afifi  3 , Tuba Esatbeyoglu  4 , Sahar S Abdelrahman  5 , Hany M Fayed  2
Affiliations

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

Marawan A Elbaset et al. Sci Rep. .

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.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Experimental design of EPO intervention in TAA-intoxicated rats.
Figure 2
Figure 2
Effect of EPO (150 and 300 IU/kg) on serum renal function tests of TAA-intoxicated rats (a) urea and (b) creatinine. Each bar represents the mean ± SE of 6 rats. * vs normal control group, @ vs TAA group, # vs EPO (150 mg/kg) at p < 0.05.EPO: Erythropoietin; TAA: thioacetamide.
Figure 3
Figure 3
Effect of EPO (150 and 300 IU/kg) on oxidative stress markers in renal tissue of TAA-intoxicated rats (a) MDA (µM/mg protein) (b) GSH (nmol/mg protein). Each bar represents the mean ± SE of 6 rats. * vs normal control group, @ vs TAA group, # vs EPO (150 mg/kg) at p < 0.05. EPO: Erythropoietin; TAA: thioacetamide.
Figure 4
Figure 4
Effect of EPO on renal content of (a) JAK2 (b) p- JAK2, (c) p- JAK2/JAK2, (d) STAT5, (e) p-STAT5, (f) p-STAT5/STAT5, (g) AMPK, (h) p-AMPK and (i) p-AMPK/AMPK in renal tissue of TAA-intoxicated rats. Each bar represents the mean ± SE of 6 rats. * vs normal control group, @ vs TAA group, # vs EPO (150 mg/kg) at p < 0.05.EPO: Erythropoietin; TAA: thioacetamide; GSH: reduced Glutathione; MDA: Malondialdehyde.
Figure 5
Figure 5
Effect of EPO on renal gene expression of (a) JAK2 and (b) PI3K of TAA-intoxicated rats. Each bar represents the mean ± SE of 6 rats. * vs normal control group, @ vs TAA group, # vs EPO (150 mg/kg) at p < 0.05.EPO: Erythropoietin; TAA: thioacetamide.
Figure 6
Figure 6
Effect of EPO on renal histopathology findings of TAA-intoxicated rats.
Figure 7
Figure 7
Effect of EPO on PERK expression in kidney tissues of TAA-intoxicated rats.
Figure 8
Figure 8
Protective effect of EPO against TAA-induced renal injury. EPO: Erythropoietin; TAA: thioacetamide; ROS: reactive oxygen species.
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