摘要
目的:观察应用抗细胞间黏附分子1单克隆抗体阻断大鼠缺血再灌注后由细胞间黏附分子1介导的的炎症反应,对缺血脑组织的保护作用。方法:实验于2003-04/2004-04在徐州医学院附属医院神经病学实验室进行。将造模成功的健康雄性SD大鼠24只随机分为3组,每组8只:①脑缺血组:线栓法建立大鼠大脑中动脉栓塞模型。②再灌注组:同前造模,于缺血6h回抽尼龙线开始再灌注。③抗细胞间黏附分子1单克隆抗体组:处理同再灌注组,再灌注同时经颈内动脉注入抗细胞间黏附分子1单克隆抗体1mg/kg。每组随机取5只大鼠于再灌注48h在麻醉状态下处死,用免疫组织化学方法观察各组大鼠脑内细胞间黏附分子1阳性血管数,苏木精-伊红染色观察大鼠脑内白细胞浸润数,炎症反应;各组剩余3只大鼠同时间麻醉状态下处死,四氮唑红测定大鼠脑梗死体积占脑半球的百分率。结果:24只大鼠进入结果分析。①脑内细胞间黏附分子1阳性血管数:抗细胞间黏附分子1单克隆抗体组低于再灌注组,与脑缺血组无差异[(298±35),(450±73),(417±46)个/mm2]。②脑白细胞浸润数:抗细胞间黏附分子1单克隆抗体组低于再灌注组和脑缺血组[(8.5±1.7),(28.7±5.9),(16.3±4.6)个,P<0.05]。③脑梗死体积占脑半球的百分率:抗细胞间黏附分子1单克隆抗体组低于再灌注组,与脑缺血组无差异[(26.4±2.5)%,(42.5±3.5)%,(36.6±4.1)%]。结论:抗细胞间黏附分子1单克隆抗体对脑缺血后所伴发的炎症反应有抑制作用;可减轻缺血后脑组织的损伤,缩小脑梗死体积,在炎症损伤环节上可延长大鼠脑梗死的溶栓治疗时间窗。
AIM： To observe the inflammatory reaction mediated by intercellular adhesion molecule-1 and protective effects on brain ischemia tissue after using anti-intercellular adhesion molecule-1 （anti-1CAM-1） monoclonal antibody to block ischemia reperfusion in rats. METHODS： The experiment was carried through in the Neurology Laboratory of the Affiliated Hospital of Xuzhou Medical College from April 2003 to Apri] 2004. Twenty-four healthy male SD rats which were successfully built were randomly divided into three groups with 8 rats in each group： ① Cerebral ischemia group： To set up the embolism models of middle cerebral artery model in rats through line-1ock method. ② Reperfusion group： To set up the ditto model and begin to reperfuse with back and forth nylon thread at ischemia 6 hours. ③ Anti-1CAM-1 monoclonal antibody group： The treatment was the same as reperfusion group. When therats were performed reperfusion they were also injected with anti-1CAM-1 monoclonal antibody 1 mg/kg through internal carotid artery. Five rats were selected randomly from every group and conducted reperfusion on them for 48 hours and were killed in drugged state, then the number of positive blood vessels in inner brain ICAM-1 in rats of each group was observed by through immunohistochemical method. The number of the leukocytic infiltrate and inflammatory reaction of inner brain in rats was observed by hematoxylin-eosin staining. In each group the remanent three rats were killed in drugged state at the same time and the percentage of cerebral infarction volume assay accounted for brain hemisphere in rats through TYC. RESULTS： All the 24 rats were involved in the analysis of results.① The number of positive blood vessels of inner brain ICAM-1： It was lower in the anti-1CAM-1 monoclonal antibody group than that in reperfusion group, and no difference with cerebral ischemia group [（298±35）, （450±73）, （417 ±46） /mm^2]. ② The number of the brain leucocyte infiltration： It was lower in the anti-1CAM-1 monoclonal antibody group than that in reperfusion group and cerebral ischemia group [（8.5±1.7）, （28.7±5.9）, （16.3±4.6）, P 〈 0.05]. ③ The percentage of cerebral infarction volume on brain hemisphere： It was lower in the anti-1CAM-1 monoclonal antibody group than that in reperfusion group, and no difference with cerebral ischem, ia group [（26.4±2.5）%, （42.5±3.5）%, （36.6±4.1）%]. CONCLUSION： The anti-1CAM-1 monoclonal antibody has inhibitive effects on the inflammatory reaction after cerebral ischemia; it can relieve the injury on brain tissue after ischemia, shorten the cerebral infarction volume, and prolong the time window of thrombolysis therapy in rats with cerebral infarction during the link of inflammation injury.
出处
《中国临床康复》
CSCD
北大核心
2005年第29期116-118,共3页
Chinese Journal of Clinical Rehabilitation
