【摘要】：全身性炎癥反應綜合征(systemic inflammatory response syndrome, SIRS)和代償性抗炎反應綜合征(compensatory anti-inflammatory response syndrome, CARS)是感染性及創(chuàng)傷性疾病并發(fā)多器官功能障礙綜合征(multiple organ dysfunction syndrome, MODS)的重要病理過程。MODS不僅有炎癥介質(zhì)過度釋放,而且還伴有內(nèi)源性抗炎介質(zhì)的不足或過度釋放,兩者均可導致炎癥反應失控,最終導致多系統(tǒng)器官衰竭(multiple systemic organ failure, MSOF)以至死亡。在炎癥反應失控而發(fā)展成MODS的病理過程中,肺臟是公認的較早發(fā)生功能障礙的器官,急性肺損傷(acute lung injury, ALI)或急性呼吸窘迫綜合征(acute respiratory distress syndrome, ARDS)即是MODS 在肺部的表現(xiàn)。 作為一種重要的炎癥介質(zhì),細胞因子在炎癥的發(fā)生發(fā)展過程中發(fā)揮著重要作用,其失控性釋放是構(gòu)成ARDS 和MODS 的主要病理學基礎。根據(jù)細胞因子在宿主防御反應中的功能不同,可將其分為兩類:促炎細胞因子和抗炎細胞因子。在炎癥反應發(fā)展的過程中,機體在釋放TNF-α、IL-1β、IL-6 等促炎細胞因子的同時,亦可分泌IL-10、IL-4 等抗炎性細胞因子以對抗炎癥反應、維持機體內(nèi)環(huán)境的穩(wěn)定�；罨膯魏�-巨噬細胞是炎癥反應中細胞因子的重要來源, G-菌菌壁的主要活性成分脂多糖(lipopolysaccharide, LPS)是誘導巨噬細胞產(chǎn)生和釋放炎癥介質(zhì)最強烈、最有效的激活物,在G-菌感染和內(nèi)毒素休克發(fā)病中發(fā)揮重要作用。 膽囊收縮素(cholecystokinin, CCK)是一種典型的腦腸肽,它不但具有胃腸激素的功能,還以神經(jīng)遞質(zhì)和神經(jīng)調(diào)質(zhì)的形式發(fā)揮著重要的作用。近年的研究表明,八肽膽囊收縮素(CCK-8)具有一定的抗炎作用,用CCK-8 預處理可使內(nèi)毒素休克(endotoxin shock, ES)大鼠平均動脈壓回升而肺動脈壓降低,并明顯減輕LPS 引起的大鼠心肌組織、肺臟、脾臟和腎臟白細胞浸潤、毛細血管血液淤積等征象,抑制體內(nèi)TNF-α、IL-1β、IL-6 等促炎因子的升高。ES 大鼠脾、肺、心臟組織及肺間質(zhì)巨噬細胞
[Abstract]:Systemic inflammatory response syndrome (systemic inflammatory response syndrome, Sirs) and compensatory anti-inflammatory response syndrome (cars) are important pathological processes of infectious and traumatic diseases complicated with multiple organ dysfunction syndrome (multiple organ dysfunction syndrome, mods). The overrelease of the mediums of the disease, It is also accompanied by insufficient or excessive release of endogenous anti-inflammatory mediators, both of which can lead to uncontrolled inflammatory response and ultimately to multiple system organ failure (multiple systemic organ failure, MSOF) and even death. In the pathological process of inflammatory reaction losing control and developing into mods, the lung is recognized as an organ with early dysfunction. Acute lung injury (acute lung injury, Ali) or acute respiratory distress syndrome (acute respiratory distress syndrome,) is the manifestation of mods in the lung. As an important inflammatory mediator, cytokines play an important role in the occurrence and development of inflammation. The uncontrolled release of cytokines is the main pathological basis of ARDS and mods. According to the different functions of cytokines in host defense response, they can be divided into two categories: pro-inflammatory cytokines and anti-inflammatory cytokines. During the development of inflammatory reaction, the body releases proinflammatory cytokines, such as TNF- 偽, IL-1 尾 and IL-6, and also produces anti-inflammatory cytokines such as IL-10, IL-4, in order to counteract the inflammatory reaction and maintain the stability of the body's internal environment. Activated monocyte-macrophages are important sources of cytokines in inflammatory reactions. Lipopolysaccharide (LPS), the main active component of G- bacteria, is the most powerful and effective activator in inducing macrophages to produce and release inflammatory mediators. It plays an important role in the pathogenesis of G-bacteria infection and endotoxic shock. Cholecystokinin (CCK) is a typical brain intestinal peptide. It not only has the function of gastrointestinal hormones, but also plays an important role in the form of neurotransmitter and neuromodulator. Recent studies have shown that cholecystokinin octapeptide (CCK-8) has a certain anti-inflammatory effect. Pretreatment with CCK-8 can increase the mean arterial pressure and decrease the pulmonary artery pressure in rats with endotoxic shock (endotoxin shock, es). Spleen and kidney leukocyte infiltration, capillary blood stasis and other signs, inhibiting the increase of inflammatory factors such as TNF- 偽, IL-1 尾 and IL-6 in vivo. Es rat spleen, lung, heart and interstitial macrophages
【學位授予單位】：河北醫(yī)科大學
【學位級別】：博士
【學位授予年份】：2005
【分類號】：R363

【引證文獻】

相關博士學位論文 前1條

1 徐錦榮;CCK-8對rTNF-α誘導RSC-364增殖和分泌功能的影響及其信號轉(zhuǎn)導機制的研究[D];河北醫(yī)科大學;2006年

相關碩士學位論文 前1條

1 白潔;CCK-8對PGE_2誘導RSC-364表達MMP-2的影響及其分子機制[D];河北醫(yī)科大學;2007年

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