本文選題：應(yīng)激障礙 + 創(chuàng)傷后　； 參考：《解放軍醫(yī)學(xué)雜志》2014年10期

【摘要】：目的研究創(chuàng)傷后應(yīng)激障礙(PTSD)狀態(tài)下,超極化激活環(huán)核苷酸門控陽(yáng)離子通道2(HCN2)與谷氨酸轉(zhuǎn)運(yùn)體-1(GLT-1)在脊髓水平協(xié)同調(diào)控內(nèi)臟高敏感性-中樞敏化的作用及機(jī)制。方法成年雌性SD大鼠隨機(jī)分為3組,即正常對(duì)照組(n=14)、PTSD內(nèi)臟高敏感模型組(n=15)、PTSD+頭孢曲松(CTX)組[給予CTX預(yù)處理,n=15)。采用連續(xù)單一應(yīng)激(SPS)聯(lián)合足底電擊刺激法建立PTSD內(nèi)臟高敏感大鼠模型。建模7d后,采用結(jié)直腸擴(kuò)張(CRD)-內(nèi)臟運(yùn)動(dòng)反射(VMR)評(píng)估各組內(nèi)臟敏感性的改變;采用CTX選擇性誘發(fā)編碼GLT-1的基因轉(zhuǎn)錄,并采用激光共聚焦及免疫熒光技術(shù)研究脊髓HCN2的表達(dá)及CTX對(duì)其的影響。結(jié)果與正常對(duì)照組比較,PTSD組脊髓HCN2表達(dá)明顯上調(diào)(78.05±6.49 vs121.12±4.85,P0.001);與PTSD組比較,PTSD+CTX組HCN2表達(dá)顯著降低(121.12±4.85 vs 98.24±5.86,P=0.012);PTSD+CTX組HCN2表達(dá)比正常對(duì)照組明顯升高(98.24±5.86 vs 78.05±6.49,P=0.024)。在20mmHg壓力下行CRD時(shí),PTSD組的AUCVMR明顯高于PTSD+CTX組(0.2913±0.0229 vs 0.2175±0.0090,P=0.005);在40mmHg壓力下行CRD時(shí),PTSD組的AUCVMR明顯高于正常對(duì)照組(0.6200±0.0278 vs 0.3786±0.0155,P0.001),亦高于PTSD+CTX組(0.6200±0.0278 vs 0.5038±0.0336,P=0.006);在60mmHg壓力下行CRD時(shí),與正常對(duì)照組比較,PTSD組AUCVMR明顯增高(0.7663±0.0262 vs 0.5271±0.0212,P0.001),同時(shí)亦明顯高于PTSD+CTX組(0.7663±0.0262 vs 0.6400±0.0245,P=0.001)。結(jié)論在PTSD內(nèi)臟高敏感狀態(tài)下,CTX可通過直接上調(diào)GLT-1表達(dá)并間接下調(diào)HCN2的表達(dá)協(xié)同發(fā)揮抗內(nèi)臟傷害性刺激的作用,HCN2-GLT-1信號(hào)通路在脊髓水平協(xié)同參與了內(nèi)臟高敏感性-中樞敏化調(diào)控作用,可能成為防止或抑制PTSD狀態(tài)下內(nèi)臟高敏感性-痛覺敏化新靶點(diǎn)之一。
[Abstract]:Objective to investigate the role and mechanism of hyperpolarization-activated cyclic nucleotide gated cationic channel 2hCN2) and glutamate transporter GLT-1 in the regulation of visceral hypersensitivity and central sensitization at spinal cord level in post-traumatic stress disorder (PTSD). Methods Adult female Sprague-Dawley rats were randomly divided into three groups: the normal control group (n = 14) and the control group (n = 15). PTSD visceral hypersensitivity rat model was established by continuous single stress (SPS) combined with plantar electric stimulation. After 7 days of modeling, the changes of visceral sensitivity in each group were evaluated by colorectal dilatation CRDD-visceral motor reflex (VMRR), and the gene transcription encoding GLT-1 was selectively induced by CTX. Laser confocal and immunofluorescence techniques were used to study the expression of HCN2 in spinal cord and the effect of CTX on it. Results compared with the normal control group, the expression of HCN2 in the spinal cord of the PTSD group was significantly up-regulated (78.05 鹵6.49 鹵4.85 vs121.12 鹵4.85), and the expression of HCN2 in the CTX group was significantly lower than that in the PTSD group (121.12 鹵4.85 vs 98.24 鹵5.86 vs 78.05 鹵6.49). The AUCVMR of PTSD group was significantly higher than that of PTSD CTX group (0.2913 鹵0.0229 vs 0.2175 鹵0.0090 P0. 005G) under 20mmHg pressure, and the AUCVMR of CRD group was significantly higher than that of normal control group (0. 6200 鹵0.0278 vs 0.3786 鹵0. 155g P0.001C), and higher than that of PTSD CTX group (0. 6200 鹵0.0278 vs 0.5038 鹵0. 336p 0.006). When 60mmHg pressure was under CRD, the AUCVMR of PTSD group was significantly higher than that of normal control group (0. 6200 鹵0.0278 vs 0.3786 鹵0. 155g P0.001g). Compared with the normal control group, the AUCVMR in the PTSD group was significantly higher than that in the PTSD CTX group (0.7663 鹵0.0262 vs 0.5271 鹵0.0212p 0.001g / L), and was significantly higher than that in the PTSD CTX group (0.7663 鹵0.0262 vs 0.6400 鹵0.0245Pu 0.001g / L). Conclusion under the condition of visceral hypersensitivity of PTSD, CTX may play a synergistic role in visceral nociceptive stimulation by directly up-regulating the expression of GLT-1 and indirectly down-regulating the expression of HCN2. HCN2-GLT-1 signaling pathway is involved in visceral hypersensitivity at spinal cord level. Armature sensitization regulation, It may be one of the new targets to prevent or suppress visceral hypersensitivity-pain sensitization in PTSD.
【作者單位】： 第三軍醫(yī)大學(xué)大坪醫(yī)院消化內(nèi)科;第三軍醫(yī)大學(xué)大坪醫(yī)院重慶野戰(zhàn)外科研究所;
【基金】：國(guó)家自然科學(xué)基金(81070298/H0307) 重慶市重點(diǎn)基金(cstc2013jjB0143)~~
【分類號(hào)】：R749.5

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本文編號(hào)：1911188