Effect of NLRP3 inflammasome on cerebral ischemia reperfusion injury of mice and the mechanism

doi:10.3969/j.issn.1002-266X.2014.25.004

Abstract：Objective To investigate the effect of NLRP 3 inflammasome in the development of cerebral ischemia reperfusion injury in mice and the mechanism .Methods All of the C57 BL/6 mice were randomly divided into two groups , 20 in each group:the control group and glyburide group .Glyburide was used as inhibitor of NLRP 3 inflammasome and a mouse model of cerebral ischemia reperfusion was established by middle cerebral artery occlusion ( MCAO ) .Ten mice of each group were subjected to MCAO to make the ischemia reperfusion models , and others underwent sham opera-tion.Glyburide 500 mg/kg was given to the mice in the glyburide group by intraperitoneal injection 30 min before surgery. After MCAO, neurological scoring and TTC staining were conducted and the ischemic infarction area was calculated .The pathological change and neuronal apoptosis in brain tissues were observed with HE staining and TUNEL staining , respec-tively.The expression of NLRP3 and cytokines ( IL-1β, IL-18) was identified by Western blotting and ELISA , respective-ly.Results The degree of brain injury in IR mice of each group was more serious than that of the sham operation group , but the IR mouse brain damage of the control group was more serious than that of glyburide group .HE staining and TUNEL staining indicated significant injuries were found in the brain tissues of IR mice , the amount of neuronal apoptosis was in-creased, and the glyburide reduced the degree of pathological injuries caused by reperfusion .Compared with the control group, the increasing degree in expression of NLRP3 protein and cytokines (IL-1β, IL-18) was significantly decreased in the glyburide group (all P<0.05).Conclusion NLRP3 inflammasome promotes the development of cerebral ischemia reperfusion injuries by increasing cytokine release and enhancing the neuron apoptosis .