Rutin attenuates neurobehavioral deficits, oxidative stress, neuro-inflammation and apoptosis in fluoride treated rats.

Studies have shown that high exposure to fluoride (NaF) induces neurotoxicity. Rutin (RUT), a citrus flavonoid, has been reported to have antioxidant, anti-inflammatory and anti-apoptotic properties. The aim of this study was to investigate the neuroprotective mechanism(s) of RUT on NaF - induced neurotoxicity. Rats were exposed to NaF alone in drinking water at 15 mg/L alone ad libitum or orally co-treated by gavage with RUT at 50 and 100 mg/kg body weight for 31 consecutive days. A video-tracking software was used to monitor the motor and locomotive behavior during a 5 - min trial time in a novel environment. Thereafter, acetylcholinesterase (AChE) activity, oxidative stress markers, pro-inflammatory cytokines and caspase - 3 activity were determined in the cerebrum and striatum. The result indicates that NaF - induced neurobehavioral deficits. RUT mediated the reversal of the neurobehavioral deficits and enhanced the exploratory profile of NaF - treated rats as supported by the track plot analyses. Moreover, RUT attenuated the NaF - induced inhibition of antioxidant enzymes and AChE activity and inhibits lipid peroxidation, neuro-inflammation and apoptosis in the cerebrum and striatum of the rats. Collectively, the present study demonstrated that RUT attenuates NaF - Induced toxicity in the cerebrum and striatum of rats via mechanisms involving enhancement of AChE activity, antioxidant status with concomitant inhibition of lipid peroxidation, neuro-inflammation and apoptosis in rats. RUT may be used as a neuroprotective agent against NaF - induced neurotoxicity.