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

Marawan A Elbaset1, Bassim M S A Mohamed2, Shaimaa A Gad2

  • 1Pharmacology Department, Medical Research and Clinical Studies Institute, National Research Centre, 33 El-Bohouth St., Dokki, P.O. 12622, Cairo, Egypt. ma.sayed@nrc.sci.eg.

Scientific Reports
|September 11, 2023
PubMed

Insights

Erythropoietin (EPO) shows therapeutic promise for kidney injury. EPO treatment in rats improved kidney function and reduced damage caused by thioacetamide (TAA), highlighting its protective effects.

Area of Science:

  • Nephrology
  • Pharmacology
  • Biochemistry

Background:

  • Kidney disease is a significant health concern with poor outcomes.
  • The kidney's role in waste removal and homeostasis is critical.
  • Thioacetamide (TAA) is a known nephrotoxic agent used to induce kidney injury in research models.

Purpose of the Study:

  • To evaluate the therapeutic potential of erythropoietin (EPO) in mitigating thioacetamide (TAA)-induced kidney injury in a rat model.
  • To investigate the molecular mechanisms underlying EPO's protective effects against nephrotoxicity.

Main Methods:

  • Induction of kidney injury in rats using thioacetamide (TAA).
  • Administration of erythropoietin (EPO) as a potential therapeutic agent.
  • Assessment of kidney function markers (serum urea, creatinine).
  • Measurement of oxidative stress markers (malondialdehyde, reduced glutathione).
  • Analysis of key signaling pathways (AMPK, JAK2/STAT5) and gene expression.
  • Histopathological examination of kidney tissues.

Main Results:

  • EPO treatment significantly improved kidney function and ameliorated elevated serum urea and creatinine levels.
  • EPO administration reduced malondialdehyde and increased reduced glutathione, indicating antioxidant effects.
  • EPO suppressed the TAA-induced increase in phosphorylated JAK2, STAT5, and AMPK.
  • EPO treatment downregulated the expression of JAK2, PI3K, and PERK genes.
  • Histopathological analysis revealed that EPO mitigated TAA-induced kidney damage.

Conclusions:

  • Erythropoietin (EPO) demonstrates significant renoprotective effects against thioacetamide-induced kidney injury in rats.
  • EPO exerts its protective effects through antioxidant, anti-inflammatory, and modulation of key signaling pathways (AMPK, JAK2/STAT5).
  • These findings suggest EPO as a potential therapeutic candidate for managing kidney injury and disease.

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