CCK-8对炎症反应中促炎及抗炎性细胞因子表达的调控机制研究
发布时间：2018-07-22 14:44
【摘要】：全身性炎症反应综合征(systemic inflammatory response syndrome, SIRS)和代偿性抗炎反应综合征(compensatory anti-inflammatory response syndrome, CARS)是感染性及创伤性疾病并发多器官功能障碍综合征(multiple organ dysfunction syndrome, MODS)的重要病理过程。MODS不仅有炎症介质过度释放,而且还伴有内源性抗炎介质的不足或过度释放,两者均可导致炎症反应失控,最终导致多系统器官衰竭(multiple systemic organ failure, MSOF)以至死亡。在炎症反应失控而发展成MODS的病理过程中,肺脏是公认的较早发生功能障碍的器官,急性肺损伤(acute lung injury, ALI)或急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)即是MODS 在肺部的表现。 作为一种重要的炎症介质,细胞因子在炎症的发生发展过程中发挥着重要作用,其失控性释放是构成ARDS 和MODS 的主要病理学基础。根据细胞因子在宿主防御反应中的功能不同,可将其分为两类:促炎细胞因子和抗炎细胞因子。在炎症反应发展的过程中,机体在释放TNF-α、IL-1β、IL-6 等促炎细胞因子的同时,亦可分泌IL-10、IL-4 等抗炎性细胞因子以对抗炎症反应、维持机体内环境的稳定。活化的单核-巨噬细胞是炎症反应中细胞因子的重要来源, G-菌菌壁的主要活性成分脂多糖(lipopolysaccharide, LPS)是诱导巨噬细胞产生和释放炎症介质最强烈、最有效的激活物,在G-菌感染和内毒素休克发病中发挥重要作用。 胆囊收缩素(cholecystokinin, CCK)是一种典型的脑肠肽,它不但具有胃肠激素的功能,还以神经递质和神经调质的形式发挥着重要的作用。近年的研究表明,八肽胆囊收缩素(CCK-8)具有一定的抗炎作用,用CCK-8 预处理可使内毒素休克(endotoxin shock, ES)大鼠平均动脉压回升而肺动脉压降低,并明显减轻LPS 引起的大鼠心肌组织、肺脏、脾脏和肾脏白细胞浸润、毛细血管血液淤积等征象,抑制体内TNF-α、IL-1β、IL-6 等促炎因子的升高。ES 大鼠脾、肺、心脏组织及肺间质巨噬细胞
[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- 伪, 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- 伪, IL-1 尾 and IL-6 in vivo. Es rat spleen, lung, heart and interstitial macrophages
【学位授予单位】：河北医科大学
【学位级别】：博士
【学位授予年份】：2005
【分类号】：R363
本文编号：2137800
[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- 伪, 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- 伪, IL-1 尾 and IL-6 in vivo. Es rat spleen, lung, heart and interstitial macrophages
【学位授予单位】：河北医科大学
【学位级别】：博士
【学位授予年份】：2005
【分类号】：R363
【引证文献】
相关博士学位论文 前1条
1 徐锦荣;CCK-8对rTNF-α诱导RSC-364增殖和分泌功能的影响及其信号转导机制的研究[D];河北医科大学;2006年
相关硕士学位论文 前1条
1 白洁;CCK-8对PGE_2诱导RSC-364表达MMP-2的影响及其分子机制[D];河北医科大学;2007年
，本文编号：2137800
本文链接：https://www.wllwen.com/yixuelunwen/binglixuelunwen/2137800.html
最近更新
教材专著
