Sinapic acid alleviates renal ischemia-reperfusion injury by regulating oxidative stress, apoptosis, and inflammation.

Abstract

Background/aim: Acute kidney injury (AKI) is a major clinical issue, frequently resulting from ischemia-reperfusion (I/R) injury. Sinapic acid (SA), a natural phenolic molecule included in numerous plant-based foods, exhibits antiapoptotic, antioxidant, and antiinflammatory properties. This study aimed to investigate the renoprotective effects of SA in an I/R-induced acute kidney injury (AKI) model.

Materials and methods: Sprague-Dawley male rats (n = 32) were randomly assigned to four groups: sham, I/R, SA 20 mg/kg, and SA 40 mg/kg. SA was administered intraperitoneally before reperfusion. Renal tissues were examined using biochemical, histopathological, and immunohistochemical methods, focusing on oxidative stress, cytokine expression, and apoptosis markers.

Results: I/R induced significant oxidative stress, elevated proinflammatory cytokines, and tubular damage. Treatment with SA, particularly at 40 mg/kg, significantly improved antioxidant defenses, reduced inflammatory cytokine levels, and attenuated tubular necrosis and apoptosis, as confirmed by decreased caspase-3 and HAVCR1 (also known as KIM-1) expression.

Conclusion: SA significantly ameliorated renal I/R injury by modulating apoptosis, inflammation, and oxidative stress. These findings support the therapeutic efficacy of SA in AKI and highlight the need for further translational research.