- The influence of rutin on fluoride – induced neurotoxicity in rat was studied.
- Rutin reversed the fluoride – induced neurobehavioral deficits in rats.
- Rutin reversed the fluoride – induced inhibition of acetylcholinesterase activity in rat cerebrum and striatum.
- Rutin enhanced antioxidant status and inhibited neuro-inflammation and apoptosis in fluoride induced rat cerebrum and striatum.
- Rutin may serves as a potential neuroprotective agent in fluoride – mediated neurotoxicity.
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.