论文部分内容阅读
目的探讨LTA诱导的延迟预适应对大鼠局灶性脑缺血/再灌注损(I/R)损伤的作用.方法采用改良Longa法制作大鼠右大脑中动脉(MCA)闭塞2 h造成局灶性脑缺血模型,恢复血液灌流24h.大鼠在施行脑缺血前24 h腹腔注射脂质胞壁酸(LTA,1 mg/kg)诱导延迟预适应,检测脑组织再灌注24 h后组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)含量以及大鼠神经症状,并用透射电镜观测大鼠大脑皮层神经细胞的超微结构改变.结果LTA预适应能明显减少脑I/R后组织中MDA的含量(P＜0.01),提高SOD的水平(P＜0.01),减轻神经细胞的超微结构损伤和保护细胞膜结构完整性,LTA预适应还能明显改善脑I/R后的神经功能,减少神经缺欠评分值(P＜0.01).LTA预适应亦能明显降低I/R导致脑组织中NO含量的升高(P＜0.01).结论LTA诱导的延迟预适应能显著减少大鼠脑组织再灌注损伤,减少脑组织坏死,其作用机制与减少脑I/R后自由基和NO毒性作用有关.“,”OBJECTIVE To explore the beneficial effects of lipoteichoic acid (LTA) -induced delayed preconditioning (PC) on reperfusion injury after middle cerebral artery occlusion in rats. METHORDS Focal cerebral ischemia/reperfusion (I/R) in rats was made by occlusion of the right middle cerebral artery (MCA) using the intra-arterial thread method for 2 h and followed by reperfusion for 24 h. The rats were pretreated with LTA (1 mg/kg, ip) 24h before the experiment, to examine the neurologic deficit by a standard neurological evaluation, and to measure the concentrations of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) in right cerebral tissues at the end of reperfusion by chromometry, to observe the ultrastructure of right cerebral tissues by electron microscope. RESULTS LTA-induced delayed PC obviously improved the neurogical deficit (P ＜ 0.01), and significantly decreased the content of MDA and increase the level of SOD in cerebral tissue at the end of reperfusion (all P ＜ 0.01). LTA pretreatment also significantly inhibited the ultrastructure of the neuron dramatic destruction after reperfusion and protected the integrity of cell body.Additionally, pretreatment with LTA obviously decreased the increase of NO concentration induced by I/R in cerebral tissues (P ＜0.01). CONCLUSION LTA-induced delayed PC can prevent brain damage caused by peroxidate reaction and reduce the destruction of ultrastructure of the neuron. The neuroprotective mechanisms of LTA pretreatment may be associated with anti-free radical effect and decreased the cytotoxic effect of NO.