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


GÜLER M. C., Ekinci Akdemir F. N., Eraslan E., TANYELİ A., Güzel Erdoğan D., Tebrizi B.

Turkish Journal of Medical Sciences, cilt.55, sa.4, ss.992-1002, 2025 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 55 Sayı: 4
  • Basım Tarihi: 2025
  • Doi Numarası: 10.55730/1300-0144.6052
  • Dergi Adı: Turkish Journal of Medical Sciences
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, MEDLINE, Veterinary Science Database, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.992-1002
  • Anahtar Kelimeler: apoptosi, inflammation, oxidative stress, renal ischemia-reperfusion, Sinapic acid
  • Atatürk Üniversitesi Adresli: Evet

Özet

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.