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目的观察环磷酰胺对大鼠脑缺血再灌注后神经功能、脑组织中肿瘤坏死因子-α(TNF-α)表达的影响。方法36只雄性SD大鼠分为假手术组和脑缺血再灌注组。脑缺血再灌注组中包括环磷酰胺治疗组和生理盐水对照组,每组按脑缺血2h后再灌注2、4、6、24h又分为4个亚组。脑缺血再灌注组于脑缺血2 h再灌注24h进行神经功能评分；并分别于再灌注后2、4、6、24h处死动物,用免疫组织化学法观察再灌注后不同时间点TNF-α的表达情况。结果(1)环磷酰胺治疗组的神经功能评价明显好于生理盐水对照组。(2)脑缺血再灌注后,脑缺血坏死区周边TNF-α的表达增多,并于24h达高峰；环磷酰胺组在相同再灌注时间点的TNF-α的表达明显低于对照组。结论脑缺血再灌注后TNF-α的表达上调,参与了脑缺血再灌注损伤的过程。环磷酰胺治疗组神经功能好于对照组,TNF-α表达少于对照组,说明环磷酰胺有抑制细胞因子表达上调,具有神经保护的作用,为该治疗应用于临床提供了理论基础。
Objective To observe the effects of cyclophosphamide on the neurological function and the expression of tumor necrosis factor-α (TNF-α) after cerebral ischemia-reperfusion in rats. Methods Thirty-six male Sprague-Dawley rats were divided into sham operation group and cerebral ischemia reperfusion group. Cerebral ischemia-reperfusion group, including cyclophosphamide treatment group and saline control group, each group after cerebral ischemia 2h and reperfusion 2, 4, 6, 24h is divided into 4 subgroups. Neurological deficit scores were measured at 2 h and 24 h after cerebral ischemia in reperfusion group. Animals were sacrificed at 2, 4, 6 and 24 h after reperfusion. Immunohistochemistry was used to observe the changes of TNF- α expression. Results (1) The neurological evaluation of cyclophosphamide group was significantly better than that of saline control group. (2) After cerebral ischemia and reperfusion, the expression of TNF-α in peripheral ischemic necrosis area increased and peaked at 24h; the expression of TNF-α in cyclophosphamide group at the same time of reperfusion was significantly lower than that in control group . Conclusion The expression of TNF-α is up-regulated after cerebral ischemia-reperfusion, which is involved in the process of cerebral ischemia-reperfusion injury. Cyclophosphamide treatment group neurological function better than the control group, TNF-αexpression less than the control group, indicating that cyclophosphamide inhibited the upregulation of cytokines, with neuroprotection, for the treatment of clinical application provides a theoretical basis.