本文關(guān)鍵詞：亞硝基化的二硫鍵異構(gòu)酶介導(dǎo)甲基苯丙胺致小鼠相關(guān)腦區(qū)α-突觸核蛋白表達(dá)升高　出處：《南方醫(yī)科大學(xué)學(xué)報(bào)》2017年10期 　論文類(lèi)型：期刊論文

  更多相關(guān)文章： 甲基苯丙胺 二硫鍵異構(gòu)酶 亞硝基化 α-突觸核蛋白 一氧化氮合酶

【摘要】：目的研究亞硝基化的二硫鍵異構(gòu)酶(PDI)對(duì)甲基苯丙胺(METH)致小鼠海馬及紋狀體區(qū)α-突觸核蛋白(α-SN)表達(dá)的影響。方法利用C57小鼠METH亞急性中毒模型,使用一氧化氮合酶(NOS)抑制劑N-硝基-L-精氨酸(L-NNA)與METH共同造模,實(shí)驗(yàn)分為對(duì)照組、L-NNA組、METH組、METH+L-NNA組。Western Blotting技術(shù)檢測(cè)各組海馬及紋狀體區(qū)內(nèi)一氧化氮合酶(NOS)、PDI及其S亞硝基化(PDI-SNO)和α-SN表達(dá)情況。一氧化氮試劑盒檢測(cè)各組一氧化氮含量。結(jié)果 METH給藥后NOS、一氧化氮含量、PDI-SNO、α-SN表達(dá)較對(duì)照組均明顯升高(P0.05);L-NNA與METH共處理后與METH組對(duì)比,NOS表達(dá)下降(P0.05),一氧化氮含量明顯減少(P0.05),能夠顯著抑制PDI-SNO表達(dá)(P0.05),伴隨α-SN表達(dá)降低(P0.05)。而MET H+L-NNA組、L-NNA組與對(duì)照組比較均無(wú)明顯差異(P0.05)。結(jié)論 METH作用后誘導(dǎo)NOS活化,一氧化氮含量升高,PDI發(fā)生顯著S亞硝基化而功能失活,導(dǎo)致相關(guān)腦區(qū)α-SN表達(dá)升高,而NOS抑制劑L-NNA能部分緩解METH神經(jīng)毒性作用。
[Abstract]:Objective to study the effect of nitrosated disulfide isomerase (PDI) on 偽 -synaptophysin (偽 -SN) in the hippocampus and striatum of mice induced by methamphetamine (METHs). Methods the subacute poisoning model of METH in C57 mice was used. Nnitro-L-arginine L-NNA), a nitric oxide synthase (NOS) inhibitor, was used to establish the model with METH. The model was divided into control group and L-NNA group. METH L-NNA group. Western Blotting technique was used to detect nitric oxide synthase (NOS) in hippocampus and striatum. The expression of PDI, PDI-SNOand 偽 -SN and the content of nitric oxide in each group were detected by nitric oxide kit. Results the contents of NOS and no were detected after METH administration. Compared with the control group, the expression of PDI-SNO and 偽 -SN increased significantly (P 0.05). Compared with METH group, L-NNA and METH decreased the expression of NOS and the content of nitric oxide (P0.05). It could significantly inhibit the expression of PDI-SNO and decrease the expression of 偽 -SN. However, the expression of 偽 -SN was decreased in MET H L-NNA group. There was no significant difference between L-NNA group and control group (P 0.05). Conclusion METH can induce the activation of NOS and increase the content of nitric oxide. In PDI, S-nitrosation and functional inactivation resulted in increased 偽 -SN expression in related brain regions, while L-NNA, an inhibitor of NOS, partially alleviated the neurotoxicity of METH.
【作者單位】： 南方醫(yī)科大學(xué)法醫(yī)學(xué)院;上海交通大學(xué)醫(yī)學(xué)院附屬新華醫(yī)院;順德職業(yè)技術(shù)學(xué)院醫(yī)藥衛(wèi)生學(xué)院;廣州市刑事科學(xué)技術(shù)研究所//廣東省法醫(yī)遺傳學(xué)重點(diǎn)實(shí)驗(yàn)室;
【基金】：國(guó)家自然科學(xué)基金(81373240) 廣東省自然科學(xué)基金(2014A030313300,2014A030310025)~~
【分類(lèi)號(hào)】：R749.64
【正文快照】： 甲基苯丙胺(METH)屬于苯丙胺類(lèi)神經(jīng)興奮劑,在 世界范圍內(nèi)被廣泛濫用,是當(dāng)前對(duì)公共衛(wèi)生和社會(huì)危害最大的毒品之一[1-2]。研究表明METH主要作用于中樞神經(jīng)系統(tǒng),結(jié)構(gòu)與兒茶酚胺類(lèi)神經(jīng)遞質(zhì)相似,主要表現(xiàn)為多巴胺等單胺類(lèi)神經(jīng)末梢的損傷,可出現(xiàn)與帕金森病等神經(jīng)退行性疾病相似的病，

本文編號(hào)：1427068