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目的探讨口服灌胃PTD-SOD对大鼠局灶性脑缺血再灌注(cerebral ischemia-reperfusion,CIR)引起的脑损伤的保护作用及机制。方法采用线栓法制作大鼠大脑中动脉闭塞再灌注模型(middle cerebral artery occlusion,MCAO),缺血2 h,再灌注24 h。于缺血前一周开始灌胃给予PTD-SOD 10,20,40 mg.kg-1,2次.d-1。对术后MCAO大鼠进行神经行为学特性观察并评分;TTC染色法测量大鼠脑梗死面积;生化法检测大鼠脑组织匀浆中SOD、GSH-Px、CAT的活力和MDA、NO的含量。HE染色观察大鼠脑组织病理改变。结果 PTD-SOD可明显改善大鼠神经行为,减少脑梗死面积,提高脑内SOD、GSH-Px、CAT的活性,降低脑组织中MDA及NO含量,减轻脑组织病理改变(P<0.05或P<0.01)。结论 PTD-SOD可减轻CIR神经细胞损伤,其机制可能与其能抗自由基损伤,减轻NO神经毒性有关。
Objective To investigate the protective effect and mechanism of oral administration of PTD-SOD on brain injury induced by focal cerebral ischemia-reperfusion (CIR) in rats. Methods Middle cerebral artery occlusion (MCAO) was established by thread occlusion in rats. The rats were subjected to ischemia 2 hours and reperfusion 24 hours. PTD-SOD 10, 20, 40 mg.kg-1, 2 times .d-1 was given intragastrically one week before ischemia. The neurological behavior of MCAO rats were observed and scored. TTC staining was used to measure the area of cerebral infarction in rats. The contents of SOD, GSH-Px and CAT, the content of MDA and NO in brain homogenate of rats . HE staining was used to observe the pathological changes of rat brain. Results PTD-SOD could significantly improve the neurological behavior, reduce the infarct size, increase the activities of SOD, GSH-Px and CAT in the brain, decrease the contents of MDA and NO in the brain tissue, and alleviate the pathological changes in brain tissue (P <0.05 or P <0.01). Conclusion PTD-SOD can reduce CIR nerve cell injury, the mechanism may be related to its ability to resist free radical damage and reduce NO neurotoxicity.