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目的研究蝎毒纤溶活性肽对大鼠脑缺血再灌注损伤的保护作用。方法采用大鼠右侧大脑中动脉阻塞(MCAO)2 h,再灌注24 h模型,造模前,蝎毒纤溶活性肽组分别静脉注射蝎毒纤溶活性肽0.1,0.2,0.4 mg·kg-1,尼莫地平组注射尼莫地平0.7 mg·kg-1,1次·d-1,连续7 d。分别以Longa′s法评定神经功能、红四氮唑(TTC)染色测定脑梗死体积及放射免疫技术检测血清炎性细胞因子TNF-α、IL-6以及IL-8等的变化。结果与模型组比较,蝎毒纤溶活性肽能明显改善大鼠MCAO后神经功能症状,缩小梗塞体积(P<0.05),并抑制血清炎性细胞因子TNF-α、IL-6及IL-8的表达(P<0.05)。结论蝎毒纤溶活性肽对大鼠脑缺血再灌注损伤有保护作用,其机制可能与抑制炎性细胞因子表达有关。
Objective To study the protective effect of scorpion venom fibrinolytic active peptide against cerebral ischemia-reperfusion injury in rats. Methods The right middle cerebral artery occlusion (MCAO) rats were used for 2 hours and reperfusion for 24 hours. Before the model was established, scorpion venom fibrinolytic active peptides were intravenously injected with 0.1, 0.2, 0.4 mg · kg -1, nimodipine was injected nimodipine 0.7 mg · kg -1,1 times · d-1 for 7 days. The neurological function was assessed by Longa’s method, the infarct volume was measured by TTC staining and the changes of serum inflammatory cytokines such as TNF-α, IL-6 and IL-8 were detected by radioimmunoassay. Results Compared with the model group, the scorpion venom fibrinolytic active peptide could significantly improve the neurological function, reduce the infarct volume (P <0.05), and inhibit the levels of serum inflammatory cytokines TNF-α, IL-6 and IL-8 (P <0.05). Conclusion Scorpion venom fibrinolytic active peptide has a protective effect on cerebral ischemia-reperfusion injury in rats, and its mechanism may be related to inhibiting the expression of inflammatory cytokines.