Neuroprotective effects of crocin via nitric oxide production against formalin-induced hippocampus and optic nerve damages in rats.

Objectives: Formalin is a potent neurotoxic in human and animal models. It was documented that crocin can inhibit inducible nitric oxide synthase expression and nitric oxide production in vitro. In vitro studies also indicate an interaction between nitric oxide and formaldehyde induced neurotoxicity. In this study, the effect of crocin, main constituent of Crocus sativus L. (Saffron) on formalin-induced hippocampus and retinal cytotoxicity was evaluated in rats.Materials Methods: Formalin was administered intraperitoneally for 5 days to induced neurotoxicity. The effect of crocin administration alone and it co-administration with formalin was evaluated on passive avoidance of male rats using passive avoidance shuttle box. Then, rat hippocampus, retinas and optic nerve were removed and sectioned, and was evaluated histologically. To determine the contribution of NO to crocin reduced hippocampal cell loss following formalin, l-arginine, the NO synthesis precursor, and a nonselective nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME) were used.Results Conclusion: The injection of rats with crocin reduced mortality, hippocampal and retinal cells and optic nerve injury induced by formalin. Also crocin reversed formalin induced impairment on passive avoidance memory performance of rats. In conclusion, our results indicated that pretreatment with crocin protected central and peripheral neuronal cells from formalin-induced damage. Results of the present study suggest that inhibition of NO synthesis may exaggerate the neurotoxic effects of formalin.