MIP-2、IL-18、IL-6、IL-10在内毒素致大鼠脑水肿中的变化及意义

发布时间：2018-05-21 18:46

本文选题：巨噬细胞炎症蛋白2 + 白介素18　；参考：《郑州大学》2005年硕士论文

【摘要】：脑水肿是中枢神经系统(CNS)感染后主要病理变化之一,主要分为细胞源性水肿和血管源性水肿。感染性脑水肿的形成机制十分复杂,影响因素繁多。目前,细胞因子被认为是免疫反应中的基本介质,在脑水肿的形成过程中具有广泛的作用,直接或间接参与炎症细胞的活化和浸润。细胞因子在体内的作用是极其复杂的,彼此之间在诱生、受体调节及生物学效应的发挥这三个水平相互影响,构成一个内容丰富,关系复杂的细胞因子网络(Cytokin Network)。近年来有研究报道在中枢神经系统炎症中有趋化因子的表达。巨噬细胞炎症蛋白2(MIP-2)是趋化因子ELR~+C×C的重要成员,来源于多种细胞,其主要生物学功能是在炎症反应中趋化和活化中性粒细胞(PMN),并且与其他细胞因子如白介素18(IL-18)、白介素6(IL-6)、白介素10(IL-10)等之间存在着复杂的相互调节的关系。本实验通过大鼠颈内动脉注入脂多糖(LPS)造成脑水肿模型,在此基础上,监测MIP-2、IL-18、IL-6、IL-10的变化,并且予以纳络酮(NAL)干扰,探讨它们的作用和相互关系,进一步阐明内毒素致大鼠脑水肿的发病机制,为临床治疗提供新的方法。方法:健康成年SD大鼠84只,雌雄不限,体重180～200g,随机分为3组,每组28只。对照组(NS组):28只,0.2ml生理盐水颈内动脉注射;内毒素组(LPS组):28只,200ug的LPS颈内动脉注射;纳洛酮组(NAL组):28只,颈内动脉注射LPS后10min、1h、2h、6h、12h及处死前2h腹腔注射纳络酮1mg/kg。每组均按观察时间分为4h、6h、12h、24h 4个时间点,每组各时间点均为7只。
[Abstract]:Brain edema is one of the main pathological changes after CNS infection, which can be divided into cellular edema and vasogenic edema. The formation mechanism of infective brain edema is very complex and the influencing factors are various. At present, cytokines are considered as the basic mediators of immune response, which play a wide role in the formation of brain edema, directly or indirectly involved in the activation and infiltration of inflammatory cells. The role of cytokines in vivo is extremely complex. The interaction of cytokines at the three levels of induction, receptor regulation and biological effects constitutes a rich and complex network of cytokines, called Cytokin Network. In recent years, it has been reported that chemokines are expressed in central nervous system inflammation. Macrophage inflammatory protein 2 (MIP-2) is an important member of the chemokine ELRC 脳 C, and is derived from a variety of cells. Its main biological function is chemotaxis and activation of neutrophil PMNs in inflammatory reactions, and there are complex interregulatory relationships between PMNs and other cytokines such as IL-18, IL-6, IL-10, and so on. The model of brain edema was established by injecting lipopolysaccharide (LPSs) into the internal carotid artery of rats. On the basis of this model, the changes of IL-6 IL-10 in MIP-2 IL-18 were monitored, and the interference of naloxone (NAL) was given to explore their role and relationship. To further elucidate the pathogenesis of endotoxin-induced brain edema in rats and provide a new method for clinical treatment. Methods: 84 healthy adult SD rats were randomly divided into 3 groups with 28 rats in each group. The control group (n = 28) was injected with 0.2ml normal saline, the endotoxin group (n = 28) was injected with 200ug of LPS, and the naloxone group (n = 28) was given intraperitoneal injection of naloxone (1mg / kg) 10 min after LPS injection for 6 h and 12 h after LPS injection. Each group was divided into 4 groups according to the observation time of 4 hours, 6 hours, 12 hours and 24 hours, and 7 rats in each group.
【学位授予单位】：郑州大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R363

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