Polydatin attenuates sodium fluoride-induced oxidative and inflammatory damage in rats

Objective: This study aimed to evaluate the protective effects of polydatin against sodium fluoride-induced oxidative and inflammatory stress in rats. Methods: A total of 35 rats were randomly divided into five groups (n = 7 per group) and treated over a 14-day period. The groups were defined as follows: Control (no treatment), NaF (600 ppm sodium fluoride in drinking water), NaF+PD25 (600 ppm NaF + polydatin 25 mg/kg body weight by oral gavage), NaF+PD50 (600 ppm NaF + polydatin 50 mg/kg), and NaF+PD100 (600 ppm NaF + polydatin 100 mg/kg). Biochemical markers of oxidative stress including malondialdehyde (MDA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), liver enzyme levels (AST, ALT, ALP) were measured using spectrophotometric methods. The expression levels of inflammatory genes (IFN-γ, TNF-α, and NF-κB) were determined using reverse transcription-polymerase chain reaction (RT-PCR). Histopathological evaluations of the liver, brain, kidneys, and testes were also conducted. Results: Sodium fluoride exposure significantly increased MDA levels and decreased GSH, CAT, and SOD levels in both serum and tissue samples (p < 0.05 to p < 0.001). Serum levels of AST, ALT, and ALP were elevated, indicating hepatic damage. Expression of inflammatory genes IFN-γ, TNF-α, and NF-κB was also upregulated in liver and kidney tissues. Polydatin treatment reversed these changes in a dose-dependent manner: MDA levels were reduced, while GSH, CAT, and SOD levels increased. Liver enzyme levels were lowered, and inflammatory gene expression was suppressed. Histopathological findings supported these results, showing that polydatin mitigated tissue damage in all examined organs. Conclusion: Sodium fluoride induced marked oxidative stress and inflammation in rats. Polydatin exhibited dose-dependent protective effects by restoring antioxidant defenses, reducing inflammation, and preserving tissue integrity, highlighting its protective potential against fluoride-induced oxidative and inflammatory damage.