博碩士論文 992204021 詳細資訊




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姓名 黃薇羽(Wei-yu Huang)  查詢紙本館藏   畢業系所 生命科學系
論文名稱 蛋白質激酶A以及蛋白質激酶Cɛ在急性轉換至慢性發炎性疼痛中扮演的角色
(Roles of Protein Kinase A and Protein Kinase Cε in the Transition from Acute to Chronic Inflammatory Pain)
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摘要(中) 尋找有效治療慢性發炎性疼痛是目前臨床研究上重要的課題。組織受損釋放大量發炎介質引起的發炎反應常常會伴隨著持續性以及慢性疼痛的發生。發炎介質會透過蛋白質激酶A以及蛋白質激酶Cɛ活化痛覺相關神經元 (nociceptor),引發痛覺過敏感行為。在前人研究中指出,在預發炎的模式中 (priming model) 蛋白質激酶Cɛ可能扮演關鍵的角色在轉換急性疼痛至慢性發炎性疼痛中。但另外利用發炎介質引發持續性的疼痛研究中發現蛋白質激酶A同時與蛋白質激酶Cɛ共同參與在急性以及慢性疼痛中,因此蛋白質激酶A以及蛋白質激酶Cɛ在實際上的發炎反應從開始急性痛到慢性發炎性疼痛的過程中是如何參與以及透過何種機制調控是目前尚未明瞭的課題,因此我藉由長期 (完全弗氏佐劑)、短期 (海藻醣)、神經內源性 (辣椒素) 發炎模式,在發炎反應的不同時間下注射蛋白質激酶A以及蛋白質激酶Cε抑制劑來探討蛋白質激酶A以及Cε參與那些階段下,以及他們透過何種路徑調控急性疼痛以及慢性疼痛之間的轉換。在長期以及短期模式中,抑制蛋白質激酶A只可以降低前期 (1-3小時) 發炎性疼痛,但抑制蛋白質激酶Cɛ可以降低後期 (4小時至16天),因此推測這樣的蛋白質激酶主導由短期疼痛轉換至長期疼痛的機制主要介於發炎後3-4小時間。在辣椒素引發的短期神經內源性發炎反應中,機械性痛覺過敏只可以受抑制蛋白質激酶Cɛ所減緩,然而熱痛覺過敏感可同時受蛋白質激酶A以及蛋白質激酶Cɛ抑制劑所降低。在神經內源性發炎反應中並無顯著的激酶主導轉換,利用定量聚合酶鏈鎖反應分析發炎後酸敏感G蛋白偶和受體基因變化,發現發炎初期抑制蛋白質激酶A活性會促使G2A基因表現增加,發炎後一天TDAG8基因表現增加的現象可以受蛋白質激酶Cɛ抑制劑作用而降低。
摘要(英) The treatment of chronic inflammatory pain continues to be a major management challenge in clinical practice. Inflammation induced by tissue injury release inflammatory mediator often accompanies persistent and chronic pain. Inflammatory mediators activate protein kinase A (PKA) or protein kinase Cε (PKCε) to sensitize pain-related nerve fibers (nociceptors), inducing behavioral hypersensitivity. Some studies have demonstrated that PKCε plays a critical role in the transition from acute to chronic pain using “hyperalgesic priming” model. However it remains unclear whether PKA is involved in such transition, when the transition occurs and what is the molecular mechanism. To address these questions, I have used three (sub-chronic, chronic, neurogenic) inflammatory pain models to explore the roles of PKA and PKCε in the transition from acute to chronic pain. In both subchronic (carrgeenan) and chronic (CFA) models, inhibiting PKA activity reduced mechanical hyperalgesia in the early state (1-3 hours), but PKCε regulated mechanical hyperalgesia in the late state (4-24 hours). The kinase-dependent swithching time was at 3-4 hours, suggesting that the transition from acute pain to chronic pain is around 3-4 hours after inflammation. In a neurogenic model, inhibition of PKCε slightly reduced capsaicin-induced mechanical hyperalgesia but not PKA. Both PKA and PKCɛ can regulate capsaicin-induced thermal hyperalgesia. Blocking PKC reduced CFA -enhanced TDAG8 gene expression. Pretreatment of PKA inhibitor enhance G2A gene expression at initiation after CFA induced inflammation.
關鍵字(中) ★ 發炎性疼痛
★ 痛覺過敏感
★ 慢性疼痛
★ 蛋白質激酶A
★ 蛋白質激酶Cɛ
關鍵字(英) ★ Inflammatory pain
★ Hyperalgesia
★ Chronic pain
★ PKA
★ PKCɛ
論文目次 目錄
中文摘要……………………………………………………….….i
英文摘要…………………………………………………………..ii
目錄……………………………………………………………….iii
圖目錄…………………………………………………................. vii
附圖目錄……………………………………………………….…..ix
表目錄………………………………………………………..x

第一章 緒論 1
1.1痛覺 (Pain) 2
1.2痛覺傳遞路徑 (Nociceptive pathway) 3
1.3發炎性疼痛 (Inflammatory pain) 4
1.3.1神經可塑性 (Neuroplasticity) 5
1.3.2發炎介質 6
1.3.3激酶 8
1.3.4受體 10
1.4發炎動物模式 13
1.4.1完全弗氏佐劑 (Complete Freund’s Adjuvant) 13
1.4.2海藻醣 (Carrgeenan) 13
1.4.3神經內源性 14
1.4.4 預發炎模式 (Priming model) 14
1.5研究動機與目的 16
第二章 材料與方法 17
2-1 實驗材料 18
2-1-1 實驗小鼠 18
2-1-2 藥品 18
2-2 實驗方法 19
2-2-1 發炎性疼痛動物模式 19
2-2-2 痛覺行為測試 19
2-2-3 RNA萃取-微量組織 20
2-2-4 cDNA合成 21
2-2-5 染色體DNA (genomic DNA) 污染檢測 21
2-2-6 聚合酶鏈鎖反應分析(Reverse transcription-PCR,RT-PCR) 22
2-2-7 瓊酯膠電泳製備及電泳分析 22
2-2-8 統計分析 22
第三章 結果 24
3.1 小鼠皮下注射海藻醣及完全弗氏佐劑引發中長期機械性痛覺過敏感現象 25
3.2 皮下注射完全弗氏佐劑引發發炎反應24小時後引發同側腳掌腫脹不會受PKA以及PKCɛ抑制劑所減緩 25
3.3抑制蛋白質激酶A可以降低弗氏完全佐劑所引起的機械性痛覺過敏感前期(0~4小時)而抑制蛋白質激酶Cɛ可以減緩後期 (>4 Hours)痛覺過敏現象 26
3.4 抑制蛋白質激酶A可以降低海藻醣所引起的機械性痛覺過敏感前期而抑制蛋白質激酶Cɛ可以減緩後期痛覺過敏現象 27
3.5抑制腺苷酸環化酶活性可以降低完全弗氏佐劑以及海藻醣所引起的機械性痛覺過敏感前期 (0~4小時) 而抑制磷酯酶以及百日咳毒素活性可以減緩後期 (>4 Hours) 痛覺過敏現象 28
3.6 皮下注射完全弗氏佐劑所會引起長持續的熱痛覺過敏感現象的熱痛覺過敏感現象 30
3.7 抑制蛋白質激酶A及蛋白質激酶Cɛ活性可以減緩完全弗氏佐劑所引起的熱痛覺過敏感現象 30
3.8蛋白質激酶Cɛ抑制劑可以降低辣椒素所引起的機械性痛覺異常現象,但蛋白質激酶A抑制劑不能 31
3.9 蛋白質激酶A抑制劑及蛋白質激酶Cɛ抑制劑可以降低辣椒素所引起的熱痛覺過敏感現象 31
3.10 完全弗氏佐劑引發發炎反應後G2A以及TDAG8基因表現增加 32
3.11完全弗氏佐劑與注射蛋白質激酶A抑制劑同時注射後90分鐘G2A基因表現增加 32
3.12發炎反應後4小時注射蛋白質激酶A以及蛋白質激酶Cε抑制劑不會影響OGR1家族基因表現變化 33
3.13抑制蛋白質激酶Cɛ活性降低TDAG8基因表現在完全弗氏佐劑引發發炎反應後1天 33
第四章 討論 34
4.1 慢性發炎引發機械性痛覺過敏感 35
4.2 蛋白質激酶A以及蛋白質激酶Cε交替參與完全弗氏佐劑引發長期機械性疼痛 36
4.2.1 發炎初期(0~3小時) 37
4.2.2發炎中期至後期(4小時-16天) 37
4.3 G蛋白轉換參與調節發炎性疼痛 38
4.4蛋白質激酶A以及蛋白質激酶Cε參與調控完全弗氏佐劑引發熱痛覺過敏 39
4.5辣椒素引發的神經內源發炎反應透過蛋白質激酶Cε調節機械痛覺過敏 40
4.6 CFA引發的發炎性疼痛可以透過PKCε調節TDAG8 41
4.7總結 42
第五章 參考文獻 43

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指導教授 孫維欣(Wei-Hsin Sun) 審核日期 2012-12-22
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