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    請使用永久網址來引用或連結此文件: http://ir.lib.ncu.edu.tw/handle/987654321/49384


    題名: 血清素受體2B在疼痛之角色;The Roles of Serotonin Receptor 2B in Pain
    作者: 孫維欣
    貢獻者: 生物科技與生醫工程中心
    關鍵詞: 研究領域:基礎醫學類
    日期: 2011-08-01
    上傳時間: 2012-01-17 18:49:20 (UTC+8)
    出版者: 行政院國家科學委員會
    摘要: 非類固醇類是一種廣為人知的抗發炎藥物,但許多研究顯示這些藥物也作用在其他非發炎反應上而產生副作用。因此,瞭解發炎性疼痛的分子機制將有助於確認特定發炎反應的作用目標,進而有助於在臨床止痛治療上及抗發炎藥物發展。發炎反應的產生,主要是因為組織受傷、感染、或腫瘤增生,使周邊感覺神經末梢和其他非神經細胞釋放化學傳遞物 (如血清素、前列腺素)所造成,並通常會造成持久的慢性疼痛。發炎時,血清素由周邊血小板或肥大細胞釋放至發炎處與其他發炎物質共同作用,造成發炎性疼痛和痛覺過敏。周邊感覺神經末梢分布多種不同的血清素受體,反應出血清素引發的疼痛的複雜性及多樣性。然而,血清素引發的疼痛是經由何種血清素受體,又如何促進疼痛, 直到現在仍不明瞭。本實驗室之前研究發現阻斷血清素受體2B/2C(5-HT2B/2C)的訊息可抑制血清素所引起的機械性痛覺過敏現象,由於周邊感覺神經末梢並無表現血清素受體2C,因此血清素可能是藉血清素受體2B(5-HT2B)的作用,來調控血清素引發的疼痛。本計劃的目的是研究5-HT2B調控血清素引發的疼痛的分子機制,來釐清血清素在發炎性疼痛中扮演的角色。其中心假說是:因為5-HT2B 傳遞血清素的訊息,而調控與引起機械性疼痛相關之離子通道,而產生機械性痛覺過敏現象。因此在發炎性疼痛中,血清素亦可藉5-HT2B來調控部份機械性痛覺過敏現象。 此計劃是具有獨創性因為這是首次研究5-HT2B 在血清素引發的疼痛中所扮演的角色。本計劃預期會產生下列結果: 瞭解5-HT2B調控機械性痛覺過敏的分子機制及5-HT2B是否參與血清素對發炎性疼痛之調控機制。本計劃所提供的知識將會有助於瞭解發炎疼痛的分子機制,進而有助於臨床止痛治療及抗發炎藥物發展。 Non-steroid anti-inflammatory drugs are well-known drugs against inflammatory pain, but also have side effects. Understanding of the molecular mechanism of inflammatory pain is important to identify specific targets for clinical treatment. Inflammation resulting from tissue injury, infection or tumor growth often produces chemical mediators (such as 5-HT, prostaglandin E2, bradykinin), inducing chronic and persistent pain. Serotonin released from mast cells or platelets in the peripheral tissues is one of important inflammatory mediators in causing pain and hyperalgesia. The presence of multiple 5-HT receptors on primary afferent nociceptors reflects 5-HT-induced pain or hyperalgesia through different receptors with distinct mechanisms. Despite the potential importance of 5-HT in hyperalgesia, the involvement of 5-HT receptor subtypes in hyperalgesia and cellular mechanisms remain to be clarified. Our preliminary experiments have found that antagonist of 5-HT2B/2C inhibits 5-HT-induced mechanical hyperalgesia. Given that 5-HT2C is not present in DRG neurons and antagonist inhibition is a short-time effect, suggesting that 5-HT2B is involved in 5-HT-induced mechanical hyperalgesia. However, whether 5-HT2B participates 5-HT-induced pain and what is molecular mechanism of 5-HT2B-mediated hyperalgesia remain unclear. The objective of this application is to elucidate the role of serotonin receptor, 5-HT2B in pain. The central hypothesis of this application is that 5-HT2B mediates 5-HT signaling to regulate ion channels related to mechanical hyperalgesia. The proposed work is innovative, as it is the first study to determine the role of 5-HT2B in pain. It is expected to yield the following outcomes: elucidation of molecular mechanism of 5-HT2B–mediated mechanical hyperalgesia and elucidation of involvement of 5-HT2B in inflammatory pain. These results will be important because they are expected to facilitate understanding of molecular mechanisms of inflammatory pain and to fundamentally advance the fields of pain research and development of new anti-inflammatory drugs. 研究期間:10008 ~ 10107
    關聯: 財團法人國家實驗研究院科技政策研究與資訊中心
    顯示於類別:[生物科技與生醫工程中心] 研究計畫

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