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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/79409


    Title: ASIC3基因的剔除調控M1/M2巨噬細胞比例以減緩坐骨神經慢性壓迫性損傷所誘發的熱痛覺過敏;ASIC3 gene deletion modulates M1/M2 macrophage ratio to attenuate thermal hyperalgesia induced by chronic constriction injury of the sciatic nerve
    Authors: 黃翊筑;Huang, Yi-Chu
    Contributors: 生命科學系
    Keywords: ASIC3;神經病變性疼痛;巨噬細胞;熱痛覺過敏;CCI
    Date: 2019-01-17
    Issue Date: 2019-04-02 14:21:48 (UTC+8)
    Publisher: 國立中央大學
    Abstract: 神經病變性疼痛是由神經系統中的原發病變或功能障礙引發或引起的疼痛。症狀包括自發性疼痛,感覺異常,感覺異常,異常性疼痛和痛覺過敏。神經病變性疼痛通常伴隨神經炎症,免疫反應,衛星神經膠質細胞 (Satellite glial cells, SGCs) 激活和神經元損失。局部組織酸中毒是調節發炎反應和誘發疼痛的主要因素。酸敏感離子通道3 (Acid-sensing ion channel 3, ASIC3) 是質子傳感受體之一,直接或間接地介導疼痛和痛覺過敏反應。然而,ASIC3參與神經病變性疼痛的相關機制尚不清楚。我已經建立了坐骨神經慢性壓迫性損傷模型(Chronic constriction injury, CCI),以探討ASIC3在神經性疼痛中的作用。我發現CCI小鼠出現了長期的機械性和熱痛覺過敏反應。ASIC3-/-小鼠從第一周開始減緩由CCI誘導的長期熱痛覺過敏,並且抑制效果維持在14W。組織化學分析顯示在CCI小鼠的受損神經中顆粒性細胞和巨噬細胞引發長期神經發炎反應。在ASIC3-/-小鼠中,巨噬細胞的總數在術後第一周增加但在第4、8周時減少。我發現剔除ASIC3基因減少了促炎性巨噬細胞(M1)的數量,但增加了抗炎症巨噬細胞(M2)的數量。因此,從我的實驗結果可以推論ASIC3可能藉由調控M1/M2巨噬細胞的比例來參與在外週神經損傷誘導的熱痛覺過敏。;Neuropathic pain is a pain initiated or caused by a primary lesion or dysfunction in the nervous system. Symptoms include spontaneous pain, dysaesthesia, paraesthesia, allodynia and hyperalgesia. Neuropathic pain often accompanies with neuroinflammation, immune responses, satellite glial cells (SGCs) activation and neuron loss. Local tissue acidosis is a major factor to regulate inflammation and induce pain. Acid-sensing ion channel 3 (ASIC3), one of proton-sensing receptors, directly or indirectly mediates pain and hyperalgesia. However, it remains unclear whether is involved in neuropathic pain. I have established a model chronic constriction injury of sciatic nerves (CCI) to explore the role of ASIC3 in neuropathic pain. I have found that CCI mice developed long-term mechanical hyperalgesia and thermal hyperalgesia. In ASIC3-/- mice, the long-term thermal hyperalgesia induced by CCI was reduced from the first week and the inhibitory effect was maintained for 14W. Histochemistry analysis of injured nerve demonstrated that CCI mice developed long-term inflammation with granulocytes and macrophages. In ASIC3-/- mice, the number of macrophages were significantly increased compared to ASIC3+/+ at the first week but decreased at 4, 8W. I have found that ASIC3 deletion decreased the number of pro-inflamatory macrophage (M1), but increased the number of anti-inflamatory macrophage (M2) after CCI surgery. Accordingly, ASIC3 may involve in thermal hyperalgesia induced by peripheral nerve injury via modulates the proportion of M1 / M2 macrophages ratio.
    Appears in Collections:[生命科學研究所 ] 博碩士論文

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