Background: Nephrotoxicity is considered one of the most serious and dose-limiting factors for restricting clinical use of Cisplatin and anticancer efficacy. Gallic acid is a non-toxic substance that has a wide range of therapeutic roles with high antioxidant activity. So, the present study aims to investigate the concurrent protective action of Gallic acid against inflammatory and oxidative damage caused by Cisplatin in rat kidneys. Material and methods: Thirty-two male albino rats were classified into four groups, eight per each as follows: Group 1 (Normal control group): without treatment. Group 2 (Gallic acid group): healthy rats were given Gallic acid. Group 3 (Cisplatin group): healthy rats were injected with Cisplatin. Group 4 (Gallic acid + Cisplatin) treated group. Kidney functions, Paraoxonase-1, and inflammatory cytokines such as Tumor Necrosis Factor α, respectively were determined. Results: Cisplatin was induced kidney damage with a high significance (P <0.001) regarding kidney function tests and the group of Cisplatin + Gallic acid demonstrated a broad range in the prevention and/or management of kidney damage with a high significance (P <0.001) compared to cisplatin group. Conclusion: Gallic acid has a protective role against kidney dysfunction and renal damage in Cisplatin therapy.

The toxicity of cisplatin (CDDP) toward the renal tubules and its severe effects on the proximal tubules limits its further use in cancer therapy. The current study was undertaken to evaluate the protective effects of gallic acid-grafted O-carboxymethyl chitosan (GA@CMCS) against nephrotoxicity induced by CDDP in rats. Renal injury was assessed in the GA@CMCS/CDDP-treated rats using kidney injury molecule-1 (KIM-1). Moreover, the levels of reduced glutathione (GSH), malondialdehyde (MDA), and nitric oxide (NO) were measured. The comet assay was performed to measure the DNA damage. The renoprotective activity of GA@CMCS was supported by histo- and immuno-pathological studies of the kidney. GA@CMCS significantly normalized the increases in kidney homogenate of KIM-1, MDA, and NO-induced by CDDP and significantly increased GSH as compared with the CDDP group. GA@CMCS also significantly protects rat kidneys from CDDP-induced histo- and immuno-pathological changes. Both biochemical findings and histo- and immuno-pathological evidence showed the renoprotective potential of GA@CMCS against CDDP-induced oxidative stress, inflammation, and renal dysfunction in rats. In conclusion, GA@CMCS has been shown to mitigate the nephrotoxicity impact of CDDP in cancer therapy.