Effects of resveratrol on cellular pyrolysis of rat brain during ischemia-reperfusion and on NLRP3 inflammatory bodies, Caspase-1 and ZO-1 in microglia

Objective: To study the effects of resveratrol on apoptosis of rat brain during ischemia-reperfusion and on NLRP3 inflammatory bodies, Caspase-1 and ZO-1 in microglia. Methods:According to the random digital table method, forty-five male Sprague-Dawley rats were divided into the sham-operated group (blank control group), cerebral ischemia-reperfusion group (IR control group) and resveratrol treatment group, with 15 rats in each group. After the establishment of cerebral ischemia-reperfusion model by suture method, the effects of different methods on the expression of apoptosis-related molecules (promoters, suppressors) in brain tissue, microglial NLRP3 inflammatory bodies, Caspase-1 and ZO-1 in SD rats were compared. Results: The content of apoptosis-related molecules (CytC, AIF, Caspase-8, Caspase-9, Fas, FasL) in the sham-operated group was significantly lower than that in IR control group and resveratrol group, and the content in IR control group was significantly higher than that in resveratrol group (P<0.05). The content of anti-apoptosis-related molecules (Livin, Survivin, XIAP) in sham-operated group was significantly higher than that in IR control group and resveratrol group, while the content of pro-apoptosis-related molecules in IR control group was significantly lower than that in resveratrol group (P<0. 05). The levels of IL-10, IL-6,TNF-α of brain tissue in resveratrol group were significantly higher than those in the control group and significantly lower than those in IR group (P<0. 05). The content of NLRP3 inflammatory body in microglia was the lowest in the sham-operated group, followed by resveratrol group, IR control group. ZO-1 content was the highest in the sham-operated group, followed by resveratrol group and IR control group. Conclusion: Resveratrol can effectively inhibit cellular pyrolysis, increase the level of NLRP3 inflammatory body and Caspase-1 and decrease the level of ZO-1 in rat brain tissue during ischemia-reperfusion, so as to play a protective role in the brain.