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目的探讨丁苯酞(NBP)预处理对脑缺血再灌注损伤大鼠神经功能缺损评分、氧化损伤和形态学的影响。方法 90只雄性SD大鼠随机分为假手术组(Sham)、模型组(IR)、NBP预处理低剂量组(NBPⅠ)、NBP预处理中剂量组(NBPⅡ)和NBP预处理高剂量组(NBPⅢ),每组18只,制造模型前7d开始灌胃给药,1次/d。线栓法制作大脑中动脉栓塞(MCAO)模型,缺血2h再灌注24h后进行神经功能缺损评分;2,3,-氯化三苯基四氮唑(TTC)染色观察脑组织梗死的情况;苏木素-伊红(HE)染色显微镜下观察脑组织形态学变化;采用羟胺法测定超氧化物歧化酶(SOD)活性,化学比色法测定谷胱甘肽过氧化物酶(GSH-PX)活性,硫代巴比妥酸(TBA)法测定丙二醛(MDA)含量。结果 (1)Sham组神经功能缺损评分为零,脑组织无梗死情况发生,神经元形态规则,脑组织中SOD、GSH-PX活性和MDA含量正常。(2)与IR组比较,NBP预处理各组大鼠神经功能评分显著降低(均P<0.01),NBPⅠ、Ⅱ、Ⅲ组神经功能评分依次递减(均P<0.05)。(3)与IR组比较,NBP预处理各组脑组织梗死体积依次减小(均P<0.05),神经元损伤减轻。(4)NBP预处理各组脑组织中SOD、GSH-PX活性明显升高,MDA含量显著减少(P<0.01);NBPⅠ、Ⅱ、Ⅲ组SOD、GSH-PX活性依次递增,MDA含量依次递减(均P<0.05)。结论丁苯酞预处理可上调SOD、GSH-PX活性,降低MDA含量,减小脑梗死体积,减轻神经元损伤,发挥对脑缺血再灌注损伤大鼠的预防性保护作用。
Objective To investigate the effect of NBP pretreatment on neurological deficit score, oxidative damage and morphological changes in rats with cerebral ischemia-reperfusion injury. Methods Ninety male Sprague-Dawley rats were randomly divided into four groups: Sham, model group (IR), NBPⅠ, NBPⅡ and NBP pretreatment high-dose group NBPⅢ), 18 rats in each group. Gavage administration was started 7 days before the model was established, once a day. The model of middle cerebral artery occlusion (MCAO) was established by the method of thread occlusion. The neurological deficit score was measured after ischemia for 2 hours and reperfusion for 24 hours. The cerebral infarction was observed by TTC staining with 2,3-triphenyltetrazolium chloride (TTC) The morphological changes of brain tissue were observed under hematoxylin-eosin (HE) staining. The activity of superoxide dismutase (SOD) was measured by hydroxylamine method. The activity of glutathione peroxidase (GSH-PX) , Thiobarbituric acid (TBA) method for the determination of malondialdehyde (MDA) content. Results (1) The score of neurological deficit in Sham group was zero. No infarction occurred in brain tissue. The morphology of neurons was normal. The activity of SOD, GSH-PX and the content of MDA in brain tissue were normal. (2) Compared with the IR group, the neurological scores of the NBP preconditioning groups were significantly decreased (all P <0.01), and the neurological scores of the NBP Ⅰ, Ⅱ and Ⅲ groups were decreased in turn (all P <0.05). (3) Compared with the IR group, the infarct volume of NBP preconditioning group decreased in turn (all P <0.05), and the neuronal damage was alleviated. (4) The activities of SOD and GSH-PX in brain tissue of NBP pretreatment group were significantly increased and MDA content was significantly decreased (P <0.01). The activities of SOD and GSH-PX in NBPⅠ, Ⅱ and Ⅲ groups were increased in turn, (All P <0.05). Conclusion Butylphthalide preconditioning can up-regulate the activity of SOD and GSH-PX, decrease the content of MDA, decrease the volume of cerebral infarction, reduce the damage of neurons and exert its preventive and protective effects on rats with cerebral ischemia-reperfusion injury.