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目的探讨超氧化物岐化酶(SOD)在p38有丝分裂素激活蛋白激酶(MAPK)介导的肢体缺血预适应(LIP)脑保护中的作用。方法永久凝闭椎动脉的Wistar大鼠,重复夹闭双侧股动脉3次(每次10min,间隔10 min)作为LIP,之后即刻夹闭双侧颈总动脉8 min造成全脑缺血。SB 203580+LIP+脑缺血组于LIP前30min侧脑室内注射p38 MAPK抑制剂SB 203580 (100μmol·L-1, 25μL)。黄嘌呤氧化酶法测定海马SOD活性,硫代巴比妥酸法测定海马丙二醛(MDA)含量,硫堇染色观察海马的组织学分级。结果LIP显著抑制脑缺血引起的海马CA1区SOD活性下降、MDA含量增加及延迟性神经元死亡。预先侧脑室注射SB 203580显著阻断LIP对缺血脑组织的上述保护作用。结论 SOD可能作为p38 MAPK的下游分子参与LIP诱导的脑缺血耐受。
Objective To investigate the role of superoxide dismutase (SOD) in the protection of limb ischemic preconditioning (LIP) induced by p38 mitogen-activated protein kinase (MAPK). Methods Wistar rats with permanent vertebral artery occlusion were occluded. The bilateral femoral arteries were occluded three times (10 min intervals and 10 min intervals) as LIP, and the bilateral common carotid arteries were immediately occluded for 8 min to induce global cerebral ischemia. SB 203580 + LIP + cerebral ischemia group was intracerebroventricularly injected with p38 MAPK inhibitor SB 203580 (100μmol·L-1, 25μL) 30min before LIP. The activity of superoxide dismutase (SOD) in hippocampus was detected by xanthine oxidase method. The content of malondialdehyde (MDA) in hippocampus was detected by thiobarbituric acid method. The histological grade of hippocampus was observed by thionine staining. Results LIP significantly inhibited the decrease of SOD activity and the increase of MDA content and delayed neuronal death induced by cerebral ischemia in hippocampal CA1 area. Preventricular injection of SB 203580 significantly blocked the protective effect of LIP on ischemic brain tissue. Conclusion SOD may be involved in LIP-induced cerebral ischemic tolerance as a downstream molecule of p38 MAPK.