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Asprosin protects against ischemia/reperfusion-induced kidney injury in mice

  • 0Department of Physiology, Faculty of Medicine, Inonu University, Malatya, Turkey.
Journal of Molecular Histology +

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August 12, 2025

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August 12, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Asprosin (ASP) protects against kidney injury caused by ischemia-reperfusion (IR). This hormone reduced inflammation, oxidative stress, and apoptosis, improving kidney function in a mouse model.

Area Of Science

  • Nephrology
  • Endocrinology
  • Pathophysiology

Background

  • Ischemia-reperfusion (IR) injury is a major cause of acute kidney injury (AKI).
  • Inflammation, oxidative stress, and apoptosis are key mechanisms in IR-induced AKI.
  • Asprosin (ASP), a fasting hormone, impacts oxidative and apoptotic pathways.

Purpose Of The Study

  • To investigate the renoprotective potential of ASP in a murine model of IR-induced AKI.
  • To evaluate ASP's effects on renal function, inflammation, oxidative stress, and apoptosis.

Main Methods

  • Male Balb/c mice were subjected to 22 minutes of renal ischemia followed by 24 hours of reperfusion.
  • Mice received intravenous ASP (1 or 10 µg/kg) or vehicle pretreatment.
  • Renal function, inflammatory cytokines (IL-1β, TNF-α), oxidative stress markers (MDA, SOD, CAT), and caspase-3 expression were assessed.
  • Kidney histopathology was evaluated using hematoxylin-eosin staining.

Main Results

  • IR significantly elevated kidney injury markers (BUN, creatinine), inflammation (IL-1β, TNF-α), oxidative stress (MDA), and apoptosis (caspase-3).
  • IR reduced antioxidant enzyme activity (SOD, CAT).
  • ASP pretreatment dose-dependently reversed these detrimental effects, improving renal function and reducing tissue damage.

Conclusions

  • Asprosin demonstrates significant renoprotective effects against IR-induced AKI in mice.
  • ASP alleviates kidney injury by mitigating inflammation, oxidative stress, and apoptosis.
  • ASP holds promise as a therapeutic agent for preventing or treating IR-induced AKI.

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