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

• Published in: Asian Pacific Journal of Tropical Biomedicine
• Main Authors: Ramakrishnan Sabitha, Kumari Nishi, Vinoth Prasanna Gunasekaran, Govindhan Annamalai, Balupillai Agilan, Mathan Ganeshan
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wolters Kluwer Medknow Publications 2019
• Subjects: p-coumaric acid; apoptosis; alcohol; cytokine; inflammation; nephrotoxicity; Arctic medicine. Tropical medicine; RC955-962; Biology (General); QH301-705.5; Arctic
• Online Access: https://doi.org/10.4103/2221-1691.258998; https://doaj.org/article/c61deccd26864e65afa70ad26c2de98b

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.