電針對(duì)炎性痛大鼠中腦邊緣鎮(zhèn)痛回路p38MAPK磷酸化水平的影響
發(fā)布時(shí)間:2018-03-07 12:39
本文選題:電針 切入點(diǎn):炎性痛 出處:《華中農(nóng)業(yè)大學(xué)》2017年碩士論文 論文類型:學(xué)位論文
【摘要】:疼痛是獸醫(yī)臨床上十分常見的癥狀,對(duì)動(dòng)物的生產(chǎn)性能產(chǎn)生極大的影響。人們?cè)噲D用不同的方法來減輕疼痛,但是無論是藥物療法、神經(jīng)阻滯療法還是手術(shù)療法,都存在效果不佳且有副作用等缺點(diǎn)。針刺療法是我國傳統(tǒng)醫(yī)學(xué)瑰寶,而電針(EA)是針刺與現(xiàn)代科技相結(jié)合的治療手段,具有安全方便、傷害性小、無副作用以及療效好等優(yōu)點(diǎn),已在全世界被廣泛用來治療疼痛。電針鎮(zhèn)痛效應(yīng)涉及神經(jīng)、體液、細(xì)胞信號(hào)轉(zhuǎn)導(dǎo)等諸多機(jī)制,電針鎮(zhèn)痛調(diào)節(jié)機(jī)制目前已成為研究熱點(diǎn)。電針通過調(diào)節(jié)中樞神經(jīng)系統(tǒng)中5-羥色胺、內(nèi)源性阿片肽等神經(jīng)遞質(zhì)和調(diào)制的釋放而產(chǎn)生鎮(zhèn)痛效應(yīng)的機(jī)制已經(jīng)比較清楚,但是電針鎮(zhèn)痛在細(xì)胞信號(hào)轉(zhuǎn)導(dǎo)層面的機(jī)制研究還比較欠缺。研究證實(shí)p38MAPK信號(hào)通路的激活在病理性疼痛神經(jīng)可塑性以及炎性反應(yīng)的發(fā)生和維持中起到了非常重要的作用,抑制p38MAPK的激活可以降低痛敏。目前有研究表明電針可以通過抑制背根神經(jīng)節(jié)以及脊髓中磷酸化p38MAPK水平達(dá)到鎮(zhèn)痛效果,然而電針是否能通過調(diào)節(jié)腦中樞尤其是中腦邊緣鎮(zhèn)痛回路中p38MAPK信號(hào)通路還尚不十分清楚。本試驗(yàn)以完全弗氏佐劑(CFA)致足底炎性痛大鼠為模型,通過研究電針對(duì)大鼠機(jī)械觸痛敏、足容積以及中腦邊緣鎮(zhèn)痛回路相關(guān)核團(tuán)中p38MAPK磷酸化水平的影響,來探討電針治療炎性痛的中樞分子機(jī)制。試驗(yàn)將144只6周齡SD大鼠隨機(jī)分為Saline組、CFA組、CFA+EA組及CFA+sham組,每組36只。Saline組于左后足底注射0.1mL生理鹽水。另外三組相同部位注射0.1mL CFA。CFA+EA組在注射后0.5h、24.5h、48.5h和72.5h,電針雙側(cè)“昆侖”(BL-60)和“足三里”(ST-36)穴,頻率2/100Hz,時(shí)間30min。CFA+sham組在相同穴位只扎針但不通電,其余處理同CFA+EA組。在1h、3h、5h、7h、25h和73h,分別使用觸覺測(cè)痛儀和足容積測(cè)定儀測(cè)定械觸痛閾和足容積。之后分別從各組取6只大鼠,灌流固定之后取腦并制石蠟切片。采用免疫酶組織化學(xué)方法檢測(cè)中腦邊緣鎮(zhèn)痛回路各核團(tuán)大鼠中腦導(dǎo)水管周圍灰質(zhì)(PAG)、伏核(ACB)、杏仁核(AMY)和韁核(Hb)磷酸化p38MAPK陽性細(xì)胞數(shù)量。結(jié)果顯示,CFA組大鼠痛閾試驗(yàn)各時(shí)間點(diǎn)均顯著低于Saline組(p0.05)。與CFA組及CFA+sham組相比,CFA+EA組大鼠的痛閾在1、3、25及73h顯著升高(p0.05)。表明電針可以使CFA炎性痛大鼠的痛閾提高,具有即時(shí)鎮(zhèn)痛效應(yīng)和累加效應(yīng)。CFA組足容積各時(shí)間點(diǎn)均顯著高于Saline組(p0.05)。與CFA組和CFA+sham組相比,CFA+EA組大鼠足容積在5~73h顯著降低(p0.05),表明電針具有抑制炎癥的作用。CFA組PAG和Hb磷酸化p38MAPK免疫陽性(p-p38MAPK-IR)細(xì)胞水平于1~5h顯著高于Saline組(p0.05),ACB和AMY于1~7h顯著高于Saline組(p0.05)。CFA+EA組p-p38MAPK-IR水平:PAG于3~5h較CFA組和CFA+sham組明顯下降(p0.05);ACB和AMY于1~7h顯著低于CFA組和CFA+sham組(p0.05);Hb于3~5h顯著低于CFA組(p0.05),于1~5h明顯低于CFA+sham組(p0.05);四個(gè)核團(tuán)均于3h開始降低至Saline組相近水平(p0.05)。顯示電針能夠調(diào)節(jié)PAG、ACB、AMY及Hb p38磷酸化水平。本研究建立CFA炎性痛動(dòng)物模型,研究電針對(duì)該模型大鼠痛閾、足容積以及PAG-ACB-AMY-Hb p-p38MAPK水平的影響。結(jié)果表明電針能夠抑制中腦邊緣鎮(zhèn)痛回路p38MAPK信號(hào)通路的激活來調(diào)節(jié)中樞敏化,降低炎性痛大鼠觸痛敏。該研究有助于全面揭示針刺鎮(zhèn)痛機(jī)理,促進(jìn)神經(jīng)科學(xué)的發(fā)展與電針治療在獸醫(yī)臨床上的應(yīng)用。
[Abstract]:The pain is very common in clinic symptoms, have a great impact on the production performance of animal. People try to use different methods to relieve the pain, but whether it is drug therapy, nerve block therapy or surgical therapy are ineffective and have side effects such as lack of points. Acupuncture is a treasure of Chinese traditional medicine. (EA) and Electro Acupuncture Acupuncture Combined with modern science and technology, the means of treatment, is safe and convenient, small damage, no side effect, good curative effect and other advantages, has been all over the world are widely used in the treatment of pain. The analgesic effect of electroacupuncture and related nerve humoral, cellular signal transduction and other mechanisms, the regulation mechanism of electroacupuncture analgesia has become a hot research topic. By adjusting the electroacupuncture in the central nervous system 5- serotonin, mechanism of endogenous opioid peptide neurotransmitter release and modulation to produce analgesic effect has been relatively clear, but the electricity 閽堥晣鐥涘湪緇嗚優(yōu)淇″彿杞灞傞潰鐨勬満鍒剁爺絀惰繕姣旇緝嬈犵己.鐮旂┒璇佸疄p38MAPK淇″彿閫氳礬鐨勬縺媧誨湪鐥呯悊鎬х柤鐥涚緇忓彲濉戞,
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