細粒徑大氣微粒暴露對於肺部氧化傷害之修飾因子---敏感性呼吸道、老化以及臭氧共同暴露

中山醫學大學機構典藏 CSMUIR > 健康管理學院 > 公共衛生學系暨碩士班 > 研究計劃 > Item 310902500/3023

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/3023

Title:	細粒徑大氣微粒暴露對於肺部氧化傷害之修飾因子---敏感性呼吸道、老化以及臭氧共同暴露
Authors:	翁瑞宏;郭崇義;龍世俊;鄭尊仁 Weng, Jui-Hung;Kuo, Chung-Yih;Lung, Shih-Chun;Cheng, Tsun-Jen
Contributors:	中山醫學院公共衛生系
Keywords:	大氣微粒;顆粒物;內毒素;老化動物;細胞激素;第六介白質;腫瘤壞死因子α Airborne particulate;Particulate matter;Endotoxin;Aging animal;Cytokine;Interleukin-6;Tumor necrosis factor
Date:	2001
Issue Date:	2010-12-06T03:23:26Z (UTC)
Abstract:	大氣微粒(Particulate matter [PM])的增加與易感受性的老年族群之疾病率、甚至死亡率具有統計相關；然而微粒暴露與健康效應的機轉，目前仍不清楚。此外，內毒素(Endotoxin)可以引發細胞在隨後的刺激下，產生更大的反應；因此，我們選擇老化及年輕大鼠來比較在單獨暴露於內毒素，或者合併之大氣微粒暴露後之肺部發炎反應的差異。粒徑小於10 m之大氣微粒是以石英纖維濾紙加以收集；年輕(年紀 20 週大)及老化年紀60週大)之雄性大鼠，被區分為為以下六組：第一組為以 PBS 處理的未暴露組；第二組為暴露粗粒徑微粒；第三組為暴露細粒徑微粒；第四組為以多醣體(Lipopolysaccharide [LPS])內毒素引發；第五組為以多醣體內毒素引發後接續暴露於細微粒。暴露後，每組三隻年輕及老化的動物被麻醉並灌洗；而細胞激素Interleukin(IL)-6及腫瘤壞死因子Tumor necrosis factor(TNF)-α濃度也以ELISA 試劑組決定，來當作肺部灌洗細胞之發炎參數。單獨暴露於細粒徑微粒的老化大鼠相較於年輕大鼠，呈現顯著較高的IL-6反應(P < 0.05, ANOVA with Tukey test)；單獨暴露於 LPS 的老化大鼠相較於年輕大鼠，也呈現顯著較高的IL-6及TNF-α表現(Ps < 0.05)。此外，老化大鼠同時暴露於 LPS 與細粒徑微粒對於 IL-6 的產生具有顯著的交互作用 (P < 0.0001)；然而，並沒有類似的 IL-6 表現在年輕大鼠中。當以 TNF- 取代 IL-6 於統計分析時，年輕及老化大鼠同時暴露於 LPS 與細粒徑微粒對於 TNF- 的產生，也呈現具有顯著的交互作用。在本研究中，單獨暴露於細粒徑微粒的老化大鼠相較於年輕大鼠，具有較高的肺部發炎反應。 Increased ambient particulate matter (PM) associated with morbidity even mortality for susceptible elders. The mechanism of ambient PM exposure and health effect remains indistinct however. Additionally, endotoxin can prime target cells so that they show a greater response to a subsequent stimulus, therefore, we selected young and old rats to compare the differences of pulmonary inflammatory response after exposure to endotoxin alone or in combination with particles. Atmospheric particulates with diameters less than 10 m were collected on quartz fiber filters. Both young (20 weeks of age) and old (60 weeks of age) male rats were divided into five groups as follows: group 1, sham-exposed controls with PBS treatment; group 2, exposed to coarse particles; group 3, exposed to fine particles; group 4, lipopolysaccharide (LPS)-primed; group 5, LPS-primed followed by fine particles exposure. After dosing, three young and old animals of each dosage group were exhaustively lavaged. The interleukin (IL)-6 and tumor necrosis factor (TNF)-？\ concentration were also determined with ELISA kits as and inflammatory parameters in lung lavaged cells. Old rats exposed to fine particle alone showed a significantly higher response in IL-6 compared with young rats (P < 0.05, ANOVA with Tukey test). Significantly higher IL-6 and TNF-？\ expressions were also found in old rats exposed to LPS alone than young rats (Ps < 0.05). Additionally, there was a significant interaction on IL-6 production between LPS and fine particle exposure (P < 0.0001) in old rats. However, there were no similar results for IL-6 expression in young rats. When IL-6 was replaced by TNF-？\ in the statistical analysis, the significant interactions between LPS and fine particle in either young or old rats were also revealed. In our study, old rats exposed to fine particle or LPS had higher pulmonary inflammatory responses than young rats.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/3023
Appears in Collections:	[公共衛生學系暨碩士班] 研究計劃

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