摘要

Considerable evidence has been accumulated to suggest that blocking the inflammatory reaction promotes neuroprotection and shows therapeutic potential for clinical treatment of ischemic brain injury. Resveratrol (Res) has been demonstrated to exhibit neuroprotective functions in cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanisms in this process and its contribution to the protection function remain unknown. The current study examined the neuroprotective effects of Res after middle cerebral artery occlusion (MCAO) in rats. MCAO for 90 min was induced in male Sprague-Dawley rats. Resveratrol (30 mg/kg) pretreatment was injected intraperitoneally 10 days prior to I/R induction. Neurological score, pathological changes, infarct ratio, brain edema and inflammation-related cytokines and mediators were estimated after operation. We found that Res prevented the impairment of neurological function and decreased the infarct volume and brain edema, compared with the sham group. The inflammation-related molecules tumor necrosis factor a (TNF-alpha) and interleukin (IL)-6 levels usually caused by (I/R) injury were significantly ameliorated by Res. Meanwhile, treatment with Res inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE(2)). Finally, Res also inhibited the upregulation of nuclear factor-kappa B (NF-kappa B). In conclusion, the neuroprotection of resveratrol preconditioning may be due in part to the suppression of the inflammatory response via regulation of NF-kappa B signaling pathway, which provided a strong evidence for a promising therapeutic agent for cerebral I/R injury through attenuation of inflammation.