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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24 h。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 investigate the effect of LTA-induced delayed preconditioning on focal cerebral ischemia / reperfusion (I / R) injury in rats. Methods The model of focal cerebral ischemia was induced by occlusion of right middle cerebral artery (MCA) in rats by modified Longa method for 24 h. Rats were intraperitoneal injected with lipoteichoic acid (LTA, 1 mg / kg) 24 h before cerebral ischemia to induce delayed preconditioning. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) and nitric oxide (NO) contents and neurological symptoms of rats were observed. The ultrastructural changes of neurons in the cerebral cortex of rats were observed by transmission electron microscopy. Results LTA preconditioning could significantly reduce the content of MDA (P <0.01), increase the level of SOD (P <0.01), alleviate the ultrastructure damage of nerve cells and protect the integrity of cell membrane structure, Adaptation can also significantly improve the neurological function after cerebral I / R and reduce the nerve deficit score (P <0.01). LTA preconditioning also significantly reduced I / R-induced increase in NO content in brain tissue (P <0.01). Conclusion Delayed preconditioning induced by LTA can significantly reduce the reperfusion injury of brain tissue and decrease the necrosis of brain tissue. Its mechanism may be related to the reduction of free radical and NO toxicity after cerebral I / R.