目的 探讨瑞舒伐他汀预处理对大鼠局灶性脑缺血再灌注后大脑中动脉血管平滑肌细胞（VSMCs）中炎性细胞因子白细胞介素（IL）-1β、IL-6、肿瘤坏死因子ɑ（TNF-α）表达的影响以及可能的机制。 方法 36只健康成年SD大鼠，雌雄不限，随机分为假手术组，局灶性脑缺血再灌注组，瑞舒伐他汀预处理组，每组12只。大脑中动脉缺血2 h再灌注24 h后， Real-time PCR及Western blotting法检测大鼠大脑中动脉VSMCs中IL-1β、IL-6和TNF-α以及核因子κB（NF-κB）mRNA和蛋白的表达。 结果 再灌注24 h后，模型组VSMCs IL-1β、IL-6 以及TNF-αmRNA和蛋白的表达明显增加，而给予瑞舒伐他汀预处理后，可明显抑制大脑中动脉VSMCs中IL-1β、IL-6和TNF-α mRNA和蛋白的高表达，同时也可发现，VSMCs中NF-κB mRNA和蛋白的表达也明显减少。 结论 瑞舒伐他汀预处理可有效抑制大脑中动脉VSMCs中IL-1β、IL-6和TNF-α mRNA和蛋白的表达，从而减轻缺血再灌注后炎症反应对脑组织的进一步损伤作用。瑞舒伐他汀预处理对IL-1β、IL-6及TNF-α的作用可能与其减少VSMCs中NF-κB的表达有关。

Objective To explore the effect and probable mechanism of rosuvastatin preconditioning on inflammatory cytokines interleukin (IL)-1β，IL-6 and tumor necrosis factor α (TNF-α) release in vascular smooth muscle cells (VSMCs) of middle cerebral artery after ischemia-reperfusion. Methods Thirty-six healthy SD rats were randomly assigned into three groups：sham operation group，focal cerebral ischemia-reperfusion group and rosuvastatin preconditioning group. There were 12 rats in each group. At the 24th hour of reperfusion after middle cerebral artery occlusion (MCAO) for 2 hours, the mRNA and protein expression of IL-1β，IL-6 and TNF-α release in VSMCs of middle cerebral artery were detected by Real-time PCR and Western blotting，respectively.Also，the mRNA and protein expression of nuclear factor κB (NF-κB) were measured by Real-time PCR and Western blotting. Results At the 24th hour of reperfusion after MCAO for 2 hours，the mRNA and protein expression of IL-1β，IL-6 and TNF-α were markedly up-regulated in rats of model group；rosuvastatin preconditioning can significantly inhibited overexpression of IL-lβ，IL-6 and TNF-α at the mRNA and protein levels. And the decreasing of mRNA and protein expression of NF-κB was also found in this study. Conclusion Rosuvastatin preconditioning can decrease the release of inflammatory cytokines IL-1β，IL-6 and TNF-α in VSMCs of MCA. It can relieve the inflammatory injury after ischemia-reperfusion in brain. The effect of rovastatin on IL-1β，IL-6 and TNF-α may be related to the reduction of the expression of NF-κB in VSMCs.