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目的探讨抗血小板溶栓素(anti-platelet thrombolysin,APT)对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法 SD大鼠120只,随机分为假手术组、模型组(缺血再灌注组)、阳性组(依达拉奉1 mg·kg-1)、血小板溶栓素高、中、低剂量组(0.02、0.01、0.005 mg·kg-1),每组20只。建立线栓法大鼠缺血/再灌注模型,采用行为学评价手段评测血小板溶栓素对局灶性脑缺血再灌注大鼠神经功能恢复的影响,探讨血小板溶栓素对血清中超氧化物歧化酶(SOD)活性、谷胱甘肽过氧化物酶(GSH-Px)活性及缺血脑组织中丙二醛(MDA)和一氧化氮(NO)含量的影响,TTC染色观察抗血小板溶栓素对脑梗死面积的影响,TUNEL法原位标记海马CA1区凋亡的神经元细胞,观察其对神经元细胞凋亡的影响。结果血小板溶栓素高、中剂量组可明显改善缺血再灌注后大鼠神经功能障碍症状、减少梗死面积;高、中、低剂量组可明显抑制机体超氧化物歧化酶、谷胱甘肽过氧化酶活性的降低;高、中剂量组明显减少脑组织中丙二醛、一氧化氮的含量,抑制缺血区神经细胞的凋亡。结论血小板溶栓素具有较好的抗脑缺血再灌注损伤作用,其机制可能与抗氧化、抑制细胞凋亡有关。
Objective To investigate the protective effect of anti-platelet thrombolysin (APT) on focal cerebral ischemia-reperfusion injury in rats and its mechanism. Methods One hundred and twenty SD rats were randomly divided into sham operation group, model group (ischemia-reperfusion group), positive group (edaravone 1 mg · kg-1), thrombolytic thrombolysis high, middle and low dose group (0.02, 0.01, 0.005 mg · kg-1), 20 in each group. To establish a rat model of ischemia-reperfusion by thread-plug method, evaluate the effect of platelet thromboxane on the recovery of neurological function after focal cerebral ischemia-reperfusion in rats by behavioral evaluation, and explore the effect of thrombolysis on the level of superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity and the content of malondialdehyde (MDA) and nitric oxide (NO) in ischemic brain tissue. The effect of CTX on the area of cerebral infarction was observed by TUNEL method. The apoptosis of neuron was observed by TUNEL method. Results High and medium doses of thrombolytic agents could significantly improve the symptoms of neurological dysfunction and reduce the infarct size in rats after ischemia / reperfusion. The levels of superoxide dismutase, glutathione Peroxidase activity decreased; high and middle dose group significantly reduce the content of malondialdehyde and nitric oxide in brain tissue, inhibit the apoptosis of ischemic nerve cells. Conclusion Platelet thrombolytic agents have better anti-cerebral ischemia-reperfusion injury, and its mechanism may be related to anti-oxidation and inhibition of apoptosis.