發(fā)布時(shí)間：2018-06-09 23:47

  本文選題：弓狀核 + 慢性胰腺炎�。� 參考：《生理學(xué)報(bào)》2016年05期

【摘要】：有報(bào)道顯示初級(jí)感覺神經(jīng)元中的硫化氫(H2S)參與內(nèi)臟痛敏的形成,但其在中樞神經(jīng)系統(tǒng)中的作用卻鮮為人知。該研究旨在探討下丘腦弓狀核(arcuate nucleus,ARC)內(nèi)H2S和其內(nèi)源性合成酶是否參與慢性胰腺炎(chronic pancreatitis,CP)腹部痛覺過敏及其潛在機(jī)制。成年雄性Sprague-Dawley大鼠胰管內(nèi)注射三硝基苯磺酸(trinitrobenzene sulfonic acid,TNBS)誘導(dǎo)產(chǎn)生CP模型,運(yùn)用von Frey filament(VFF)評(píng)測(cè)大鼠腹部對(duì)機(jī)械刺激的反應(yīng)頻率,運(yùn)用Western blot檢測(cè)ARC內(nèi)蛋白表達(dá)水平。TNBS注射4周后ARC內(nèi)胱硫醚-β-合成酶(cystathionineβ-synthetase,CBS)表達(dá)顯著上調(diào),而胱硫醚-γ-裂解酶(cystathionine-γ-lyase,CSE)的表達(dá)沒有明顯改變;CP顯著提高了NMDA受體Glu N2B亞單位的磷酸化水平,而總Glu N2B不變;CP也顯著上調(diào)了蛋白激酶Cγ(PKCγ)在ARC的表達(dá)。ARC內(nèi)微量注射CBS的抑制劑O-(羧甲基)羥胺半鹽酸鹽(AOAA)能顯著降低CP大鼠的腹部疼痛,也翻轉(zhuǎn)了CP大鼠ARC中p-Glu N2B和PKCγ的上調(diào);ARC內(nèi)微量注射Glu N2B抑制劑或PKC特異性抑制劑白屈菜赤堿能顯著減輕CP大鼠的腹部痛覺過敏,PKC特異性抑制劑能減少p-Glu N2B表達(dá)。總之,以上數(shù)據(jù)表明,CP引起了ARC內(nèi)CBS的上調(diào),并可能通過PKCγ介導(dǎo)了Glu N2B的活化,參與CP痛覺過敏。本研究在一定程度上揭示了CP痛覺過敏產(chǎn)生的中樞機(jī)制,并有助于發(fā)現(xiàn)CP疼痛治療的新靶標(biāo)。
[Abstract]:It has been reported that hydrogen sulfide (H _ 2S) in primary sensory neurons is involved in the formation of visceral pain sensitivity, but its role in the central nervous system is not well known. The aim of this study was to investigate whether H _ 2S and its endogenous synthase in the arcuate nucleus arcuate of hypothalamus are involved in abdominal hyperalgesia in chronic pancreatitis (chronic pancreatitis) and its underlying mechanism. Adult male Sprague-Dawley rats were induced to produce CP by intraductal injection of trinitrobenzene sulfonic (TNBs). The frequency of abdominal response to mechanical stimulation was evaluated by von Frey filamentus. The expression of cystathionine 尾 -synthetase (CBS) was significantly up-regulated by Western blot, but the expression of cystathionine- 緯 -lyase (CSE) did not change significantly. The phosphorylation level of Glu N2B subunit of NMDA receptor was significantly increased by CP. Total Glu N2B invariant CP also significantly up-regulated the expression of protein kinase C 緯 -PKC 緯 in ARC. Microinjection of O-carboxymethyl hydroxylamine hemihydrochlorate AOAA into ARC could significantly reduce abdominal pain in CP rats. The up-regulation of p-Glu N2B and PKC 緯 in ARC of CP rats was also reversed. Microinjection of Glu N2B inhibitor or PKC-specific inhibitor of PKC into ARC could significantly reduce the expression of p-Glu N2B in abdominal hyperalgesia of CP rats. In conclusion, the above data suggest that CP may induce the up-regulation of CBS in ARC and may be involved in CP hyperalgesia through PKC 緯 mediated activation of Glu N2B. To some extent, this study reveals the central mechanism of CP hyperalgesia and helps to find new targets for CP pain therapy.
【作者單位】： 蘇州市疼痛基礎(chǔ)研究和臨床治療重點(diǎn)實(shí)驗(yàn)室蘇州大學(xué)神經(jīng)生物學(xué)和生理學(xué)系神經(jīng)科學(xué)研究所;
【基金】：supported by grants from the National Natural Science Foundation of China(No.31271258,81230024,81471137 and 31300909) the Science and Technology Development Plan of Suzhou Municipality,Jiangsu Province,China(No.SYS201037 and SYS201102) the Priority Academic Program Development of Jiangsu Higher Education Institutions,Jiangsu Province,China
【分類號(hào)】：R576

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1 Vandenberghe J.;Vos R.;Persoons P. ;J. Tack;趙菊輝;;內(nèi)臟高敏感性消化不良患者的痛覺過敏:疼痛特異性通路抑或多模式通路的致敏作用?[J];世界核心醫(yī)學(xué)期刊文摘(胃腸病學(xué)分冊(cè));2005年10期

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