【摘要】：目的：本研究通過建立大鼠坐骨神經(jīng)慢性壓迫性損傷模型(chronic constriction injury of the sciatic nerve model,CCI),運(yùn)用分子生物學(xué)技術(shù),研究Y一氨基丁酸(gamma-aminobutyric acid,GABA)受體在神經(jīng)病理性疼痛大鼠背根神經(jīng)節(jié)(dorsal root ganglion,DRG)上的表達(dá)改變,并探討其發(fā)生機(jī)制,為進(jìn)一步揭示神經(jīng)病理性疼痛的發(fā)生機(jī)制提供一定的實(shí)驗(yàn)理論依據(jù)。 方法：1)制備CCI模型,選擇雄性SD大鼠(n=30),隨機(jī)分為三組,即正常對(duì)照組(n=10)、假手術(shù)組(n=10)和CCI組(n=10)。假手術(shù)組只暴露坐骨神經(jīng)不予任何處理,CCI組在坐骨神經(jīng)結(jié)扎4-0鉻制羊腸線,分別在實(shí)驗(yàn)后0d、1d、3d、5d、7d、9d、11d、14d進(jìn)行熱板實(shí)驗(yàn),記錄熱刺激縮足潛伏期(paw withdrawal thermal latency, PWTL);取三組大鼠L4-6 DRG神經(jīng)元進(jìn)行分子生物學(xué)實(shí)驗(yàn),應(yīng)用RT-PCR技術(shù)和Western-blot技術(shù)檢測(cè)正常對(duì)照組、假手術(shù)組、CCI組GABR-AR的基因和蛋白表達(dá)改變并進(jìn)行比較。 結(jié)果：1)神經(jīng)病理性疼痛大鼠手術(shù)側(cè)的熱刺激縮足反射潛伏期(PWTL)比正常組明顯縮短(p0.05)2)通過RT-PCR方法從mRNA水平檢測(cè)GABA-AR的α2和γ2受體亞單位CCI組、正常組和假手術(shù)組的表達(dá)情況,得出結(jié)果為：CCI組的表達(dá)量下降,假手術(shù)組表達(dá)量高于正常對(duì)照組亞單位,差異有統(tǒng)計(jì)學(xué)意義(P0.05)3)通過Western blot方法從蛋白水平檢測(cè)GABA-AR的α2和γ2受體亞單位假手術(shù)組、正常組和CCI組,經(jīng)電泳成像分析系統(tǒng)掃描定量顯示,CCI組的表達(dá)量下降,假手術(shù)組表達(dá)略升高,與RT-PCR結(jié)果相一致。 結(jié)論：神經(jīng)病理性疼痛時(shí),GABA-AR的基因和蛋白水平下調(diào),GABA在初級(jí)感覺傳入終末產(chǎn)生的突觸前抑制作用被減弱,從而異化了傷害性信息的傳遞。
[Abstract]:Objective: to establish a rat model of chronic compression injury of sciatic nerve (chronic constriction injury of the sciatic nerve model,CCI) and to study Y-aminobutyric acid (gamma-aminobutyric acid,) by molecular biology. The expression of GABA receptor in dorsal root ganglion (dorsal root ganglion,DRG) of rats with neuropathic pain was changed, and its mechanism was discussed, which provided some experimental theoretical basis for further revealing the mechanism of neuropathic pain. Methods: 1) CCI model was established and male SD rats (n 鈮，

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