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目的在大鼠脑缺血再灌注模型中研究大蒜素抑制中枢神经系统参与免疫调节的小胶质细胞活化以及小胶质细胞释放炎症因子的效应。方法采用大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)的神经炎症模型缺血30 min后再灌注,用Western blot技术检测缺血皮质区在第1天和第3天小胶质细胞活化情况和白介素1-β(IL-1β)的表达水平变化,缺血再灌注模型脑室注射大蒜素后用Western blot和实时荧光定量PCR技术检测小胶质细胞标记物IBA-1和IL-1β的蛋白及mRNA表达水平的变化。离体实验中,用大蒜素预处理BV2细胞后再进行氧糖剥夺处理(oxygen glucose deprivation,OGD),观察IL-1β的蛋白和mRNA水平的变化。结果大鼠缺血再灌注模型中,缺血皮质区的小胶质细胞活化水平在第1、3天显著升高,IL-1β表达水平显著上升(P<0.05);大蒜素处理后,缺血皮质区的小胶质细胞的活化水平显著下降(P<0.05),IL-1β的蛋白表达以及mRNA水平显著下调(P<0.05)。对BV2细胞用大蒜素预处理再进行OGD处理后,IL-1β的蛋白表达和mRNA水平显著下降(P<0.05)。结论在脑缺血再灌注模型中,大蒜素可能通过抑制小胶质细胞活化以及抑制小胶质细胞释放IL-1β等细胞因子发挥抗炎作用。
Objective To study the effect of allicin on the activation of microglial cells involved in immunoregulation and the release of inflammatory cytokines by microglial cells in rat cerebral ischemia-reperfusion model. Methods The neuroinflammation model of middle cerebral artery occlusion (MCAO) was reperfused 30 min after ischemia, and the activation of microglia on day 1 and 3 of ischemic cortex was detected by Western blot. The expression of interleukin 1 -β (IL-1β) was detected by Western blotting and real-time fluorescence quantitative PCR after injecting allicin into the ventricle of ischemia-reperfusion model. The protein and protein expressions of microglial markers IBA-1 and IL- Changes in mRNA expression levels. In vitro, BV2 cells were pretreated with allicin and then oxygen glucose deprivation (OGD) was performed to observe the changes of IL-1β protein and mRNA levels. Results The microglial activation in ischemic cortex increased significantly on day 1 and 3, and the level of IL-1βincreased significantly (P <0.05) after ischemia-reperfusion in rats. After allicin treatment, The activated level of microglia in the blood cortex decreased significantly (P <0.05), and the protein expression of IL-1β and mRNA level were significantly down-regulated (P <0.05). After BV2 cells were pretreated with allicin and then treated with OGD, the protein expression and mRNA level of IL-1β were significantly decreased (P <0.05). Conclusion Allicin may play an anti-inflammatory role by inhibiting the activation of microglia and inhibiting the release of IL-1β and other cytokines by microglia in cerebral ischemia-reperfusion model.