p-Coumaric acid ameliorates ethanol–induced kidney injury by inhibiting inflammatory cytokine production and NF–κB signaling in rats

Abstract

Objective: To examine the effects of p-coumaric acid on ethanol-induced kidney injury in Swiss Wistar rats. Methods: Ethanol (25% v/v) was used to induce nephrotoxicity in rats. p-Coumaric acid was orally administered at 50, 100, or 200 mg/kg body weight. The levels of oxidative parameters were determined; pro-inflammatory biomarkers were analyzed by Western blotting and apoptotic protein was analyzed by immunohistochemistry. Results: Ethanol treated rats showed decreased levels of antioxidants and aberrant production of pro-inflammatory cytokines (IL-6, IL1P, TNF-α), NF-κB activation and imbalance of pro- and anti-apoptotic proteins (Bcl-2, Bax, caspase 3). Meanwhile, jp-coumaric acid restored antioxidant levels and decreased the levels of inflammatory cytokines, NF-κB, and pro- apoptotic proteins and increased Bcl-2 expression. Conclusions: jp-Coumaric acid ameliorates ethanol-induced kidney injury by restoring antioxidant production and suppressing cellular apoptosis and inhibiting NF-κB expression. jp-Coumaric acid should be further investigated as a promising candidate for ethanol-induced kidney toxicity.

Keywords

• p-coumaric acid
• apoptosis
• alcohol
• cytokine
• inflammation
• nephrotoxicity