本文選題：巨噬細(xì)胞炎癥蛋白2 + 白介素18�。� 參考：《鄭州大學(xué)》2005年碩士論文

【摘要】：腦水腫是中樞神經(jīng)系統(tǒng)(CNS)感染后主要病理變化之一,主要分為細(xì)胞源性水腫和血管源性水腫。感染性腦水腫的形成機制十分復(fù)雜,影響因素繁多。目前,細(xì)胞因子被認(rèn)為是免疫反應(yīng)中的基本介質(zhì),在腦水腫的形成過程中具有廣泛的作用,直接或間接參與炎癥細(xì)胞的活化和浸潤。 細(xì)胞因子在體內(nèi)的作用是極其復(fù)雜的,彼此之間在誘生、受體調(diào)節(jié)及生物學(xué)效應(yīng)的發(fā)揮這三個水平相互影響,構(gòu)成一個內(nèi)容豐富,關(guān)系復(fù)雜的細(xì)胞因子網(wǎng)絡(luò)(Cytokin Network)。近年來有研究報道在中樞神經(jīng)系統(tǒng)炎癥中有趨化因子的表達(dá)。巨噬細(xì)胞炎癥蛋白2(MIP-2)是趨化因子ELR~+C×C的重要成員,來源于多種細(xì)胞,其主要生物學(xué)功能是在炎癥反應(yīng)中趨化和活化中性粒細(xì)胞(PMN),并且與其他細(xì)胞因子如白介素18(IL-18)、白介素6(IL-6)、白介素10(IL-10)等之間存在著復(fù)雜的相互調(diào)節(jié)的關(guān)系。本實驗通過大鼠頸內(nèi)動脈注入脂多糖(LPS)造成腦水腫模型,在此基礎(chǔ)上,監(jiān)測MIP-2、IL-18、IL-6、IL-10的變化,并且予以納絡(luò)酮(NAL)干擾,探討它們的作用和相互關(guān)系,進(jìn)一步闡明內(nèi)毒素致大鼠腦水腫的發(fā)病機制,為臨床治療提供新的方法。 方法:健康成年SD大鼠84只,雌雄不限,體重180～200g,隨機分為3組,每組28只。對照組(NS組):28只,0.2ml生理鹽水頸內(nèi)動脈注射;內(nèi)毒素組(LPS組):28只,200ug的LPS頸內(nèi)動脈注射;納洛酮組(NAL組):28只,頸內(nèi)動脈注射LPS后10min、1h、2h、6h、12h及處死前2h腹腔注射納絡(luò)酮1mg/kg。每組均按觀察時間分為4h、6h、12h、24h 4個時間點,每組各時間點均為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.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363

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本文編號：1920331