氯离子转运体在神经病理性疼痛大鼠背根神经节上表达的研究

发布时间：2018-01-01 17:01

本文关键词：氯离子转运体在神经病理性疼痛大鼠背根神经节上表达的研究　出处：《中国疼痛医学杂志》2016年08期 　论文类型：期刊论文

更多相关文章： NKCC KCC 神经病理性疼痛 DRG

【摘要】：目的:为了探讨氯离子转运体的表达及其功能在神经病理性疼痛的产生和维持中的作用。方法:建立大鼠坐骨神经压迫模型(chronic constriction injury,CCI);检测大鼠热刺激缩足反射潜伏期(thermal withdrawal latency,TWL);应用免疫组化、Western Blot技术检测钠-钾-氯共转运体1(sodium-potassium-chloride co-transorter 1,NKCC1)和钾-氯共转运体2(potassium-chloride co-transorter2,KCC2)在CCI模型背根神经节(dorsal root ganglion,DRG)神经元上表达的改变;应用氯离子荧光探针MQAE(N-Ethoxycarbonylmethyl-6-methoxyquinolinium bromide)检测DRG神经元氯离子浓度的变化。结果:(1)CCI组大鼠TWL较正常对照组明显缩短(P0.01,n=10),至术后21天测试结束仍较明显(P0.05,n=10)。假手术组与正常组差异无统计学意义。(2)正常情况下,NKCC1微弱表达于DRG大、中、小型神经元,KCC2未见表达。CCI模型术后第7天、14天、21天,NKCC1表达增加,KCC2未见表达。(3)CCI组大鼠术后第7天DRG、NKCC1阳性细胞计数、中型神经元显著增加(P0.01,n=1000);术后第14天,中、小型神经元增加(P0.01,n=1000);术后第21天,中型神经元增加(P0.01,n=1000)。(4)CCI术后14、21天DRG神经元NKCC1蛋白表达显著增加。(5)CCI术后7、14天DRG神经元中氯离子浓度明显升高(P0.05,n=1000)。结论:神经病理性疼痛发生时,NKCC1在DRG神经元表达异常增加,引起细胞内Cl-浓度升高,继而可能参与了介导初极感觉外周末梢去极化(primary afferent depolarization,PAD)或/和诱发初极感觉中枢末梢端的背根反射(dorsal root reflexes,DRRs)引发痛觉过敏和异常疼痛产生。
[Abstract]:Objective: To investigate the expression of chloride ion transporter and its function in the role of generation and maintenance of neuropathic pain. Methods: to establish the rat model of sciatic nerve compression (chronic constriction, injury, CCI); rats were detected the thermal withdrawal latency (thermal withdrawal, latency, TWL); immunohistochemical detection of sodium Western Blot potassium chloride cotransporter 1 (sodium-potassium-chloride co-transorter 1, NKCC1) and potassium chloride cotransporter 2 (potassium-chloride, co-transorter2, KCC2) in dorsal root ganglion (dorsal CCI model root ganglion, DRG) on the expression of neuronal changes; application of chlorine ion fluorescent probe MQAE (N-Ethoxycarbonylmethyl-6-methoxyquinolinium bromide) to detect the changes of DRG neurons of chloride ion concentration. Results: (1) CCI in TWL group compared with normal control group was significantly shortened (P0.01, n=10), and 21 days after the operation is still the end of the test Obviously (P0.05, n=10). There was no significant difference between normal group and sham operation group (2). Under normal circumstances, NKCC1 weak expression in DRG, and small neurons, no KCC2 expression for seventh days,.CCI model after 14 days, 21 days, increase the expression of NKCC1, no KCC2 expression (3.) CCI rats after seventh days of DRG, NKCC1 positive cell count, medium neurons increased significantly (P0.01, n=1000); fourteenth days after operation, small neurons increased (P0.01, n=1000); twenty-first days after operation, medium-sized neurons increased (P0.01, n=1000). (4) the expression of 14,21 after CCI. DRG neurons of NKCC1 protein increased significantly. (5) the concentration of chloride ion in DRG neurons increased significantly in 7,14 days after CCI (P0.05, n=1000). Conclusion: neuropathic pain occurs, the expression of NKCC1 in DRG neurons caused by abnormal increase in intracellular Cl- concentration increased, and the following may be involved in the very early weekend feeling mediated shoot depolarization (primary affere NT depolarization, PAD) or / and / and the dorsal root reflex (dorsal root reflexes, DRRs) induced at the terminal end of the primary sensory Center (DRRs) causes hyperalgesia and abnormal pain.

【作者单位】：新疆石河子大学医学院/新疆地方与民族高发病教育部重点实验室;新疆石河子大学医学院第一附属医院;新疆医科大学厚博学院;
【基金】：国家自然科学基金(31260247) 兵团博士基金项目(2010JC16) 兵团医药科技攻关计划(2012BA021)
【分类号】：R741
【正文快照】： 神经病理性疼痛(neuropathic pain,NP)是指由躯体感觉神经系统的损伤或疾病所直接引起的疼痛,NP的发病率较高,在普通人群的发生率约为7%,对个体和社会造成很大的负担。NP的发病机制复杂、病理过程繁多、临床表现多变,且可累及神经系统各部位。为揭示NP的发生机制,在疼痛和镇痛

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