黑苏嘎-25对大鼠脑缺血再灌注损伤的影响

目的：本文采用黑苏嘎-25药物预处理的方法，通过局灶性脑缺血再灌注（MCAO）Wistar 大鼠模型，观察神经功能的缺损程度，测定脑梗死的体积，检测血清中 TNF-α、IL-1β表达水平的变化，探讨黑苏嘎-25对大鼠脑缺血再灌注损伤的保护作用机制。方法取清洁级健康 Wistar 大鼠60只，分为假手术组、模型未治疗组、黑苏嘎-25低剂量组、黑苏嘎-25中等剂量组、黑苏嘎-25高剂量组，用药组动物灌胃给药7天，制备 MCAO 大鼠模型，通过行为学判断神经功能缺损评分、组织病理学测定脑梗死面积、酶联免疫吸附（ELISA）法检测血清中 TNF-α、IL-1β水平，采用SPSS11．0系统进行数据分析处理，神经功能缺损评分用 Wilcoxon 秩和检验法，检测数据在组间表达的变化用单因素方差分析，P ＜0．05表示有显著性差异，具有统计学意义。结果黑苏嘎-25能减少局灶性脑缺血再灌注大鼠的神经功能缺损评分及脑梗死的面积，降低局灶性脑缺血后血清中 TNF-α、IL-1β水平。结论黑苏嘎-25对脑缺血再灌注损伤具有保护作用，其作用机制与降低脑组织中 TNF-α、IL-1β含量有关。

The Effects of Heisuga-25 on Cerebral Ischemic Reperfusion Injury of Rats

Objective Thrombolysis,antiplatelet and anticoagulant therapy are the effective methods currently,and reperfusion injure will happen after the treatment of recanalization,in which inflammatory responses play an important role.This study investigate the protection mechanism of Heisuga-25 through which test the expression level of TNF-α, IL-1βin serum in Wistar rat cerebral ischemic reperfusion injury model by preprocessing and observing nerve function injury and measuring cerebral infarction.Methods 60 clean health male Wistar rats were divided into control group, model group,Heisuga-25 low-dose group,Heisuga-25 medium dose group and Heisuga-25 high dose group,drug lavage 7 days,preparing rat focal cerebral ischemia reperfusion injury model,judging nerve function score through behavior、measuring cerebral infarction area by histopathology and testing the level of TNF-α、IL-1βin serum through ELISA,an-alyzing data using SPSS 13.0 software package,using Wilcoxon sun of ranks in nerve function score.using single factor＆amp;nbsp;analysis of variance among groups,P 〈0.05 means the difference has statistical significance.Results Heisuga-25 could reduce the nerve function score of rat with focal cerebral ischemic and cerebral infarction area,and lower the level of TNF-α,IL-1βin serum after focal cerebral ischemic.Conclusion Heisuga-25 have protective effect to cerebral ischemic reperfusion injury,and the mechanism of action is related to reducing the content of IL-1βin brain tissue.