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目的 观察奥扎格雷钠 (OS)对缺血预处理诱导的脑缺血耐受作用及核因子 κB表达的影响。 方法 4 5只SD大鼠随机分为 3组 :预处理 +OS组、预处理组、假手术组 ,每组 15只 ,分别在 2h大脑中动脉缺血 (MCAO)前 3d给予 10min的缺血预处理、缺血预处理 +OS或假手术 ,MCAO后 2 2h处死 ,比较各组间脑梗死体积、脑含水量及核因子 κB的表达。 结果 与预处理组相比 ,预处理 +OS组梗死体积缩小更为明显 [(93 75± 13 4 0 )mm3 与 (130 92± 14 5 9)mm3 ,P <0 0 5 ) ];脑水肿缺血侧进一步减轻 [(79 4 3± 0 79) %与 (81 6 6± 0 99) % ],非缺血侧为 (75 76± 0 91) %与(76 95± 0 78) % ,两组比较 ,均为P <0 0 5 ;核因子 κB表达亦进一步降低 (6 9 2 0± 5 6 3与 81 16±7 33,P <0 0 5 )。 结论 OS可增强缺血预处理所诱导的脑缺血耐受作用 ,抑制核因子 κB的激活 ,二者具有叠加效应。
Objective To observe the effect of ozagrel sodium on ischemic preconditioning induced cerebral ischemic tolerance and nuclear factor κB expression. Methods 4 5 SD rats were randomly divided into 3 groups: pretreatment + OS group, pretreatment group and sham operation group, with 15 rats in each group. The animals were given ischemia 10 min at 2h before MCAO Pretreatment, ischemic preconditioning + OS or sham operation were performed at 2h after MCAO. The infarct volume, brain water content and the expression of NF-κB in each group were compared. Results Compared with the pretreatment group, infarct volume in the pretreatment + OS group was more narrowed (93 75 ± 134 mm 3 vs (130 92 ± 14 5 9) mm 3, P 0 05); cerebral edema (79 4 3 ± 0 79)% and (81 6 6 ± 0 99)%] in the ischemic side and 75 76 ± 0 91 and 76 95 ± 0 78% in the nonischemic side, Both groups were P <0 05, and the expression of NF-κB was further decreased (69 2 0 ± 5 6 3 vs 81 16 ± 7 33, P 0 05). Conclusion OS can enhance the ischemic tolerance induced by ischemic preconditioning and inhibit the activation of nuclear factor kappa B, which has a superposition effect.