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    題名: 在小鼠發炎疼痛模式中研究電針足三里穴位對鈉離子通道表現的影響
    To investigate the effect of electroacupuncture at Zusanli (ST36) acupoint on expression of sodium channels in mice inflammation pain model
    作者: 陳香霓;Chen, Hsiang-Ni
    貢獻者: 針灸研究所碩士班
    關鍵詞: 電針;發炎疼痛;鈉離子通道;足三里穴位;Electroacupuncture;Inflammation pain;sodium channels;Zusanli (ST 36) acupoint
    日期: 2012-07-24
    上傳時間: 2012-08-31 16:32:18 (UTC+8)
    出版者: 中國醫藥大學
    摘要: 目的
    鈉離子通道與神經的興奮性有關,尤其是在初級傳入神經元的痛覺傳導上扮演了重要的角色,在10種鈉離子通道的分型中以Nav 1.7、Nav 1.8及Nav 1.9與疼痛較具高度相關性,最近研究指出在carrageenan的發炎模式下,背根神經節中可發現到Nav 1.7和Nav 1.8的表現量增加,但Nav 1.9的變化則不明顯。電針已被廣泛運用在疼痛治療上,先前研究指出電針可以引發鴉片?、腺?酸等神經傳導物質釋放來達到止痛的效果,然而電針止痛與鈉離子通道的關係卻很少被探討,因此我們使用小鼠發炎疼痛模式來研究電針足三里穴位的止痛效果以及電針對於鈉離子通道表現的影響。
    方法
    我們將18隻ICR母鼠分成控制組、發炎組及電針組,連續4日在足三里以1mA、2Hz電針15分鐘,觀察疼痛行為的變化,並在第4日取下同側第3、4、5腰椎的背根神經節,分析鈉離子通道的表現。
    結果與結論
    研究結果顯示電針可明顯降低機械性及溫度性的疼痛行為,並可調降Nav 1.7及Nav 1.8在發炎模式中的過度表現,但Nav 1.9則無顯著性差異。推論電針足三里減輕發炎疼痛的療效機轉,和調控鈉離子通道中Nav 1.7與Nav 1.8的表現相關,但與Nav 1.9則較無相關性。
    Aim
    Voltage-gated sodium channels (Navs)are crucial in modulating neuron excitability especially in nociceptive primary afferent to transduction pain signal. Of all the ten sodium channels, Nav 1.7,Nav 1.8 and Nav 1.9 channels are involved in several pain models. Recent studies have reported that Nav 1.7, Nav 1.8 but not Nav 1.9 can be up-regulated during carrageenan-induced inflammatory pain in dorsal root ganglia (DRG). Acupuncture is highly used and known to ameliorate pain sensation by releasing opioid and adenosine. In this study, we examined the curative effect on acupuncture in inflammatory pain and relationship with Nav sodium channels.
    Method
    We used 18 ICR female mice which divided into control, inflammatory and electroacupuncture groups. Animals receiving electroacupuncture (EA) 15 minutes/day for 4 consecutive days. Then we collected the ipsilateral L3-5 DRGs and analyzed the changes of sodium ion channels.
    Result and Conclusion
    Our results showed that EA at Zusanli acupoint at 2Hz stimulation reduced mechanical pain from inflammatory pain. Noticeable, the expression of Nav 1.7 and Nav 1.8 were increased at 4 day time and further attenuated by 2Hz EA stimulation. The results can not be observed in Nav 1.9 sodium channels by both immunohistochemistry and Western blot technique in a distinct population of DRG neurons. These results demonstrate that EA at Zusanli reduced carrageenan-induced inflammatory pain by reducing Nav 1.7 and Nav 1.8 overexpression rather than Nav 1.9 in DRGs.
    顯示於類別:[針灸研究所] 博碩士論文

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