本文選題：大氣混合污染物 + 大鼠��； 參考：《吉林大學(xué)》2008年碩士論文

【摘要】： 目的大氣污染已成為目前影響人類健康的主要環(huán)境問題之一。已有的文獻(xiàn)報(bào)道僅限于某種或某類大氣污染物對(duì)肺損傷機(jī)制的研究,而大氣污染對(duì)肺的損傷是由多種混合污染物所致。本實(shí)驗(yàn)?zāi)M大氣污染現(xiàn)狀,旨在探討大氣顆粒污染物(particulate matter,PM)和多種氣體混合物對(duì)呼吸道損害的共同作用,揭示肺炎性損傷的可能機(jī)制。方法本研究通過建立大氣混合污染物(PM10、SO2、NO2、CO)導(dǎo)致大鼠肺損傷的動(dòng)物模型,應(yīng)用ELISA方法測(cè)定支氣管肺泡灌洗液(Bronchoalveolar lavage fluid,BALF)中促炎和抗炎細(xì)胞因子含量的變化及觀察超微結(jié)構(gòu)的改變。結(jié)果在急性炎癥反應(yīng)的早期,染毒組大鼠BALF中細(xì)胞因子含量高于對(duì)照組。染毒1d時(shí)IL-8表達(dá)顯著高于對(duì)照組(P0.05);染毒15d、30d組細(xì)胞因子明顯低于1d組,尤為顯著的是IL-1、IL-6、IFN-γ、TNF-α(P0.05)。各細(xì)胞因子間相關(guān)分析結(jié)果顯示促炎因子(IL-1、IL-8)與抗炎因子(IL-13、IL-10)均呈中等程度正相關(guān),提示IL-1是促炎因子中代表性較好的指標(biāo);抗炎因子IL-13與促炎因子IL-1和抗炎因子IL-4均呈中等程度正相關(guān),提示IL-13是抗炎因子中代表性較好的指標(biāo)。大鼠染塵染毒后,氣管纖毛擺動(dòng)功能減弱、喪失,使分泌物及異物清除障礙,造成炎性損傷,導(dǎo)致纖毛及胞體不斷損傷脫失,通氣不暢,并引起肺組織的炎癥反應(yīng)和呼吸損失,伴有早期硬化改變;肺泡上皮漸進(jìn)性損傷,形態(tài)學(xué)變化與染塵染毒時(shí)間相一致,最終發(fā)展為肺實(shí)變,殘存肺組織為代償性氣腫。結(jié)論在大氣混合污染物所致急性炎癥反應(yīng)的早期,染毒組大鼠支氣管肺泡灌洗液中細(xì)胞因子含量高于對(duì)照組;不同染毒時(shí)間,支氣管肺泡灌洗液中細(xì)胞因子的含量1d組表達(dá)最明顯,15d、30d組細(xì)胞因子的含量呈逐漸下降趨勢(shì),炎癥反應(yīng)趨于平穩(wěn);支氣管肺泡灌洗液中促炎細(xì)胞因子IL-1、抗炎細(xì)胞因子IL-13可作為大氣混合污染物所致急性炎癥反應(yīng)的較好標(biāo)志。
[Abstract]:Objective Atmospheric pollution has become one of the major environmental problems affecting human health. The existing literature reports are limited to the study of the mechanism of lung injury caused by one or some kind of atmospheric pollutants, and the damage of air pollution to the lung is caused by a variety of mixed pollutants. The purpose of this experiment is to simulate the present situation of air pollution and to explore the interaction between particulate matterfly (PMM) and various gas mixtures on respiratory tract damage, and to reveal the possible mechanism of pneumonic injury. Methods the animal model of lung injury induced by air mixed pollutant (PM10) so _ 2SO _ 2O _ 2CO was established in this study. The changes of pro-inflammatory and anti-inflammatory cytokines in bronchoalveolar lavage (BALFF) and ultrastructural changes were measured by ELISA method. Results in the early stage of acute inflammatory reaction, the cytokines content in BALF of the exposed group was higher than that of the control group. The expression of IL-8 was significantly higher than that of the control group at day 1, and the cytokines in the group treated for 30 days were significantly lower than those in the control group, especially in the group of IL-1, IL-6, IFN- 緯, TNF- 偽, P0.05. The results of correlation analysis among cytokines showed that IL-8) was positively correlated with IL-13 (IL-10), suggesting that IL-1 is a representative index of proinflammatory factors. Anti-inflammatory factor IL-13 was positively correlated with proinflammatory factor IL-1 and anti-inflammatory factor IL-4, suggesting that IL-13 was a representative index of anti-inflammatory factor. After exposure to dust, the function of tracheal cilia swinging was weakened and lost, which caused secretion and foreign bodies to clear obstacles, caused inflammatory injury, caused continuous damage to cilia and cell bodies, lost ventilation, and caused inflammatory reaction and respiratory loss in lung tissue. Accompanied by early sclerosing changes, alveolar epithelial progressive injury, morphological changes consistent with the time of exposure to dust, the final development of pulmonary consolidation, residual lung tissue for compensatory emphysema. Conclusion in the early stage of acute inflammatory reaction induced by mixed air pollutants, the cytokines content in bronchoalveolar lavage fluid of rats in the exposed group was higher than that in the control group. Cytokines in bronchoalveolar lavage fluid the expression of cytokines in bronchoalveolar lavage fluid (BALF) was the most obvious in 1d group. The inflammatory cytokines IL-1and anti-inflammatory cytokines IL-13 in bronchoalveolar lavage fluid can be used as a good marker of acute inflammation induced by mixed air pollutants.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2008
【分類號(hào)】：R363

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本文編號(hào)：1938069