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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/71419


    Title: 抑制酸敏感受體TDAG8或ASIC3基因表現降低坐骨神經慢性壓迫性損傷所誘發的機械性痛覺過敏現象;Inhibition of TDAG8 or ASIC3 gene expression reduces mechanical hyperalgesia induced by chronic constriction injury of the sciatic nerve
    Authors: 鄧志宇;Teng,Chih-Yu
    Contributors: 生命科學系
    Keywords: 酸敏感受體
    Date: 2016-07-26
    Issue Date: 2016-10-13 13:03:15 (UTC+8)
    Publisher: 國立中央大學
    Abstract: 根據全球市場調查從2007年到2015年全球將會有1.5億人將受到長期性疼痛所困
    擾,而其中就有3到4.5%是屬於神經性疼痛的部分。在臨床神經性疼痛的治療上目前
    扔然受到巨大的挑戰。為了協助治療以及藥物的開發了解神經性疼痛的相關機制是必不可少的。而在前人的實驗中發現,神經性疼痛的小鼠會造成一個長達八天的異常性疼痛,並且也會增加ASIC3基因的表現。且在其他研究中表示,中性粒細胞在小鼠受傷後8小時內有增加的趨勢並且在24小時達到高峰。雖然發炎性疼痛與神經性疼痛的臨床特點有很大的不同,但是有研究說到在周邊的神經局部發炎現象在神經性疼痛的發展中扮演著重要的角色。在實驗中我利用在坐骨神經慢性壓迫性損傷模型(CCI)發現可以造成小鼠一個長期的機械性痛覺過敏現象現象並且能維持4個月之久。在此同時我們也發現了神經的退化現象。我們利用降低基因表現以及基因剔除的方法在小鼠上加以研究。我們的研究發現降低TDAG8的表現量可延遲由CCI所導致的機械性痛覺過敏現象,但特別的是在ASIC3基因被剔除的小鼠中卻能抑制這種由CCI所造成的機械性痛覺過敏現象。另外在坐骨神經上,在降低TDAG8基因的表現後可增加由CCI所導致的前兩週免疫細胞數量,但是在ASIC3剔除的小鼠中卻能抑制這種由CCI所導致的發炎現象。而且另一方面我們也確定了蛋白激酶A及蛋白激酶Cε也參與了由CCI所誘發的機械性痛覺過敏感現象。詳細的機制將進一步進行探討。
    ;According to global market analysis in 2007-2015, 1.5 billion people suffer from chronic pain with 3-4.5 % of population in neuropathic pain. The treatment of neuropathic pain continues to be a major management challenge in clinical practice. Understanding of the molecular mechanism of neuropathic pain is essential to identify potential drug targets for clinical treatments. Previously mice with neuropathic pain showed allodynia for 8 days, and ASIC3 immunoreactivity is up-regulated in DRG neurons. In other studies, neutrophils around the injury site increases substantially within 8 hours, and peaks at 24 hours. These studies suggest that the local inflammation of peripheral nerves and proton-sensing genes may play an important role in neuropathic pain. In this study, I used the model of peripheral mononeuropathy by chronic constriction injury (CCI) of the sciatic nerve, we have found that CCI mice developed long-term (at least 4 month) mechanical hypersensitivity and inflammation. Nerve degeneration was also found. We then generated TDAG8 knockdown(KD) and ASIC3 knockout(KO) mice to study the roles of the genes in neuropathic pain. We found that knockdown of TDAG8 delayed the onset of mechanical hyperalgesia induced by CCI. ASIC3 KO mice inhibited the late phase of CCI-induced mechanical hyperalgesia. Granulocytes cells were increased in TDAG8 KD mice in the first two weeks of CCI. Macrophages were decreased in ASIC3 KO mice in the late phase of CCI.
    Appears in Collections:[生命科學研究所 ] 博碩士論文

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