Fipronil-induced kidney injury in mice and its attenuation with p-coumaric acid

Abstract Background Fipronil is a new, broad-spectrum phenylpyrazole pesticide used in agriculture veterinary medicine to control insects, fleas and ticks. The excessive use of fipronil, due to its prolonged half-life and bioaccumulation properties, poses potential environmental, human and animal risks. P-coumaric acid is a natural dietary polyphenolic compound with antioxidant and anti-inflammatory properties. The present study aimed to investigate the ameliorative effect of p-coumaric acid on fipronil-induced acute kidney injury. The mice were divided into three groups (vehicle/control, fipronil challenged @ 25 mg/kg bodyweight and fipronil challenged @ 25 mg/kg bwt + p-coumaric acid-treated @ 100 mg/kg bodyweight groups). Hematological, kidney function biomarkers, oxidative stress parameters like lipid peroxidation, superoxide dismutase and catalase, gene expression of NF-κβ2 and histopathology were studied. Results Fipronil administration caused a significant increase in blood urea nitrogen and creatinine. A significant increase in oxidative stress, gene expression of NF-κβ2 as well as downregulation of antioxidant enzymes along with histopathological changes such as degeneration, necrosis of tubular epithelial cells, atrophied renal corpuscles and mononuclear infiltration were observed on fipronil administration. Administration of p-coumaric acid against fipronil caused decreased serum kidney function biomarkers and oxidative stress, decreased gene expression of NF-κβ2, improved the antioxidant enzyme levels and mitigated the structural changes induced by fipronil. Conclusion Thus p-coumaric acid ameliorates the fipronil-induced kidney injury in mice through attenuation of structural changes, oxidative stress, inflammation and restoration of kidney enzyme levels.