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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 鄭尊仁(Tsun-Jen Cheng) | |
| dc.contributor.author | Hsin-Yuan Cheng | en |
| dc.contributor.author | 程欣源 | zh_TW |
| dc.date.accessioned | 2021-05-14T17:42:13Z | - |
| dc.date.available | 2017-09-14 | |
| dc.date.available | 2021-05-14T17:42:13Z | - |
| dc.date.copyright | 2015-09-14 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-08-19 | |
| dc.identifier.citation | 1. Block, M.L. and L. Calderon-Garciduenas, Air pollution: mechanisms of neuroinflammation and CNS disease. Trends in Neurosciences, 2009. 32(9): p. 506-516.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/4433 | - |
| dc.description.abstract | 流行病學與毒理學研究皆有發現懸浮微粒不僅對心血管系統有影響，亦可能會對中樞神經系統產生負面的影響。多數的毒理學研究顯示其可能的機制為神經發炎反應進而造成行為改變。在本研究中，我們利用柴油引擎微粒 (DEPs) 探討急性暴露對中樞神經系統的毒性，也利用大氣細懸浮微粒 (PM2.5) 探討亞慢性暴露對中樞神經系統的影響。
本研究分為兩個部分，第一部分，C57BL/6 小鼠以氣管灌注的暴露方式暴露柴油引擎微粒，一周後進行莫式水迷津測試，再分別以學習期的逃脫時間、移動距離、累積相對距離和測試期的區域停留時間、區域經過次數、平均相對距離檢驗小鼠的空間學習與記憶能力。動物犧牲後以H&E染色進行腦組織病理檢驗。第二部分，C57BL/6 小鼠則以呼吸暴露的方式暴露大氣細懸浮微粒12周 (3個月)，暴露完後一周進行莫式水迷津測試，同樣計算小鼠的空間學習與記憶能力。另外，小鼠藉由H&E染色進行腦組織病理檢驗。 第一部分研究結果顯示急性暴露於柴油引擎微粒會使小鼠於莫式水迷津學習期的表現較差，需要較長的逃脫時間與移動距離才能找到平台，累積相對距離也較長。腦組織病理檢驗未在暴露組與控制組間發現顯著差異且在正常範圍內。第二部分研究中，12周大氣細懸浮微粒暴露的平均質量濃度為11.9 μg/ m3。低濃度亞慢性呼吸暴露於大氣細懸浮微粒後，同樣在莫式水迷津學習期中發現其對小鼠的表現有所影響。小鼠的腦組織病理檢驗未在暴露組與控制組間發現顯著差異且在正常範圍內。 過去的研究發現懸浮微粒暴露後的行為變化可能與神經發炎有關，我們發現急性暴露於柴油引擎微粒或低濃度亞慢性呼吸暴露於細懸浮微粒都可以在莫式水迷津的學習期發現小鼠的表現有所變化，未來需要進一步的生化檢驗、腦部發炎細胞染色與組織病理檢驗去探討相關機制並驗證行為實驗的結果。 | zh_TW |
| dc.description.abstract | Epidemiological and toxicological studies have shown that particulate matter may not only have adverse effects in the cardiovascular system but also in the central nervous system (CNS). Most toxicological studies suggested that particulate matter may cause neuroinflammation and behavioral changes. Here, we used diesel exhaust particles (DEPs) to explore its acute CNS toxicity and also used ambient fine particles (PM2.5) to discuss sub-chronic exposure induced CNS toxicity.
There are two parts in this study. In the first part of study, C57BL/6 mice were given DEPs by intratracheal instillation. One week after exposure, Morris water maze was conducted. Escape latency, distanced moved and cumulative distance from the center of platform quadrant or platform in acquisition phase, percentage of time spent in target area, area crossing and average proximity from the center of platform quadrant or platform were calculated to examine spatial learning and memory. Histopathological examination was then conducted in the brain using H&E stain. In the second part of study, C57BL/6 mice were exposed to ambient PM2.5 by inhalation for 12 weeks (3 months). Morris water maze was then conducted one week after the end of exposure. Spatial learning and memory ability were tested. Histopathological examination was also conducted in the brain using H&E stain. In the first part of study, results in Morris water maze test showed that acute exposure to DEPs may impair performance in acquisition phase. Mice required longer escape latency and distance moved to find the platform. Cumulative distance from the center of platform quadrant or platform was also longer. Mice histopathological examination found no significant difference between exposure and control group and was within normal limit. In the second part of study, the mean mass concentration for exposed ambient PM2.5 was 11.9 μg/ m3 during the exposure duration. Sub-chronic exposure to low concentration ambient PM2.5 may also impair performance in acquisition phase in Morris water maze test. Histopathological examination found no significant difference between exposure and control group and was within normal limit. Previous studies found that behavioral changes after PM exposure may associated with neuroinflammation. We found that both acute exposure to DEPs and low concentration sub-chronic exposure to ambient PM2.5 may affect performance in acquisition phase in Morris water maze test in mice. Further biochemical examination, inflammatory cells staining in the brain and detailed histopathological were required to explore the mechanism and support current findings in behavioral changes. | en |
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| dc.description.tableofcontents | 中文摘要 i
Abstract ii Contents iv List of Tables vii List of Figures viii Chapter 1 Introduction 1 1.1 Background 1 1.2 Objectives 2 Chapter 2 Literature review 3 2.1 Particulate matter 3 2.2 Particulate matter induced cardiovascular effects and mechanism 4 2.3 Possible mechanism in particulate matter induced CNS effects 5 2.4 Morris water maze and related neuroanatomy 7 2.5 Epidemiological studies in particulate matter related CNS effects 8 2.6 Toxicological studies in particulate matter induced CNS effects 9 2.7 Susceptibility to particulate matter in CNS effects 12 Part 1. Study of central nervous toxicity induced by diesel exhaust particles (DEPs) 13 Chapter 3 Materials and Methods 14 3.1 Study protocol 14 3.2 Animals 16 3.3 Acute diesel exhaust particles (DEPs) exposure methods 16 3.4 DEPs exposure schedule 17 3.5 Morris water maze test 17 3.6 Histopathology 19 3.7 Statistics 19 Chapter 4 Results 20 4.1 Mice body weight 20 4.2 Acquisition phase of Morris water maze test 20 4.3 Probe test of Morris water maze test 22 4.4 Histopathology 23 Chapter 5 Discussion 24 5.1 DEPs dose and effects in neurofunctions 24 5.2 DEPs characterization and DEPs effects 25 5.3 CNS effects induced by DEPs 26 5.4 Mechanism involved in DEPs induced CNS effects 27 5.5 Spatial learning and memory 28 5.6 Limitations 29 Part 2. Study of central nervous toxicity induced by ambient fine particles (PM2.5) 30 Chapter 6 Materials and Methods 31 6.1 Study protocol 31 6.2 Animals 32 6.3 Ambient PM2.5 exposure 32 6.4 Ambient PM exposure monitoring and characterization 32 6.5 Ambient PM2.5 exposure schedule 34 6.6 Morris water maze test 34 6.7 Histopathology 35 6.8 Statistics 35 Chapter 7 Results 36 7.1 Mice body weight 36 7.2 PM2.5 and PM1 exposure monitoring and characterization 36 7.3 Acquisition phase of Morris water maze test 37 7.4 Probe test of Morris water maze test 37 7.5 Histopathology 38 Chapter 8 Discussion 39 8.1 Ambient PM exposure concentration and characterization 39 8.2 CNS effects induced by PM 40 8.3 Mechanism involved in PM induced CNS effects 42 8.4 Spatial learning and memory 43 8.5 Limitations 44 Chapter 9 Conclusions 45 References 46 | |
| dc.language.iso | en | |
| dc.subject | 大氣細懸浮微粒 (PM2.5) | zh_TW |
| dc.subject | 空間學習與記憶 | zh_TW |
| dc.subject | 柴油引擎微粒 (DEPs) | zh_TW |
| dc.subject | 莫式水迷津 | zh_TW |
| dc.subject | 呼吸暴露 | zh_TW |
| dc.subject | 氣管灌注 (I.T.) | zh_TW |
| dc.subject | Spatial learning and memory | en |
| dc.subject | Diesel exhaust particles (DEPs) | en |
| dc.subject | Intratracheal instillation (I.T.) | en |
| dc.subject | ambient fine particles (PM2.5) | en |
| dc.subject | Inhalation | en |
| dc.subject | Morris water maze | en |
| dc.title | 懸浮微粒對中樞神經系統的毒性研究 | zh_TW |
| dc.title | Central Nervous System Toxicity Induced by Particulate Matter | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 吳焜裕,田履黛,陳達夫 | |
| dc.subject.keyword | 柴油引擎微粒 (DEPs),氣管灌注 (I.T.),大氣細懸浮微粒 (PM2.5),呼吸暴露,莫式水迷津,空間學習與記憶, | zh_TW |
| dc.subject.keyword | Diesel exhaust particles (DEPs),Intratracheal instillation (I.T.),ambient fine particles (PM2.5),Inhalation,Morris water maze,Spatial learning and memory, | en |
| dc.relation.page | 100 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2015-08-19 | |
| dc.contributor.author-college | 公共衛生學院 | zh_TW |
| dc.contributor.author-dept | 職業醫學與工業衛生研究所 | zh_TW |
| 顯示於系所單位： | 職業醫學與工業衛生研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-104-1.pdf | 5.11 MB | Adobe PDF | 檢視/開啟 |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。