Neuroprotective effects of resveratrol against traumatic brain injury in rats: Involvement of synaptic proteins and neuronal autophagy

Traumatic brain injury (TBI) involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death, leading to long-term cognitive deficits, and effective therapeutic strategies targeting neuronal death remain elusive. The present study aimed to determine whether the administration of resveratrol (100 mg/kg) was able to significantly enhance functional recovery in a rat model of TBI and whether resveratrol treatment was able to upregulate synaptic protein expression and suppress post-TBI neuronal autophagy. The results demonstrated that daily treatment with resveratrol attenuated TBI-induced brain edema and improved spatial cognitive function and neurological impairment in rats. The expression of synaptic proteins was downregulated following TBI and this phenomenon was partly reversed by treatment with resveratrol. In addition, resveratrol was observed to significantly reduce the levels of the autophagic marker proteins, microtubule-associated protein light chain 3-II and Beclin1, in the hippocampus compared with the TBI group. Therefore, these results suggest that resveratrol may represent a novel therapeutic strategy for TBI, and that this protection may be associated with the upregulation of synaptophysin, postsynaptic density protein 95 and the suppression of neuronal autophagy.