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蛋白激酶C在大鼠慢性炎性痛维持中的作用:与背根神经节Nav1.8表达的关系 被引量:1

Role of protein kinase C in maintenance of chronic inflammatory pain in rats: the relationship with expression of Navl. 8 in dorsal root ganglion
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摘要 目的评价蛋白激酶c(PKC)在大鼠慢性炎性痛维持中的作用及其与背根神经节Navl.8表达的关系。方法清洁级健康雌性sD大鼠30只,体重180-220g,采用随机数字表达分为3组(n=10):对照组(C组)、慢性炎性痛组(CIP组)和PKC抑制剂组(P组)。C组大鼠右后足底每天注射生理盐水20μ1.连续14d;CIP组大鼠每天足底注射前列腺素E,(PGE,)100ng,连续13d,制备大鼠慢性炎性痛模型,第14天足底注射二甲基亚砜20jxl;P组大鼠足底注射PGE,100ng,连续13d,第14天足底注射PKC抑制剂GF109203X 100nmol/20μl。于注射前1d、末次注射后1、3、7和14d(T1-4)时测定右后足机械缩足反应阈(MWT)。随后处死大鼠取L4,5节段背根神经节,通过免疫荧光和Westernblot法检测背根神经节Nav1.8表达。结果与C组比较,CIP组和P组T1-4时MWT降低,CIP组背根神经节Nav1.8表达上调(P〈0.05);与CIP组比较,P组T4时MWT升高,背根神经节Nay1.8表达下调(P〈0.05)。结论背根神经节PKC激活后Navl.8表达上调参与了大鼠慢性炎性痛的维持。 Objective To evaluate the role of protein kinase C in the maintenance of chronic in-flammatory pain in rats and the relationship with the expression of Navl. 8 in the dorsal root ganglion (DRG). Methods Thirty pathogen-free healthy female Sprague-Dawley rats, weighing 180-220 g, were divided into 3 groups using a random number table: control group (group C) , chronic inflammatory pain group (group CIP) and PKC inhibitor group (group P). Normal saline 20 μl was injected into the plantar surface of the fight hindpaw every day for 14 consecutive days in group C. Prostaglandin E2 100 ng was in-jected into the plantar surface of the right hindpaw every day for 13 consecutive days to establish the model of chronic inflammatory pain, and dimethyl sulfoxide 20 μl was injected into the plantar surface of the fight hindpaw on 14th day in group CIP. Prostaglandin E2 100 ng was injected into the plantar surface of the fight hindpaw every day for 13 consecutive days, and PKC inhibitor GF109203× 100 nmol/20 μd was injected in-to the plantar surface of the right hindpaw on 14th day in group P. The mechanical paw withdrawal threshold (MWT) was measured at 1 day before injection (T0) and 1, 3, 7 and 14 days after the last injection (Tm.4). The DRGs of the lumbar segment (L4,5) were removed for determination of Navl. 8 expression u-sing immunofluorescence and Western blot. Results Compared with group C, the MWT was significantly decreased at T4 in CIP and P groups, and the expression of Navl. 8 in DRGs was significantly up-regulated in group CIP (P〈0.05). Compared with group CIP, the MWT was significantly increased at T4, and the expression of Navl. 8 in DRGs was down-regulated in group P (P〈0. 05). Conclusion Up-regulated ex-pression of Navl. 8 after PKC activation in DRGs is involved in the maintenance of chronic inflammatory pain in rats.
作者 杨鹏举 袁峰 夏莉 白倩 董铁立 Yang Pengju;Yuan Feng;Xia Li;Bai Qian;Dong Tieli(Department of Anesthesiology, Second Affiliated Hospital of Zhengzhou University, Zhengzhou 450014, Chi- rut)
出处 《中华麻醉学杂志》 CAS CSCD 北大核心 2018年第2期209-211,共3页 Chinese Journal of Anesthesiology
基金 河南省基础与前沿技术研究计划项目(122300410403) 河南省科技厅科技攻关项目(182102310450)
关键词 蛋白激酶C 炎症 疼痛 神经节 钠通道 Protein kinase C Inflammation Pain Ganglia spinal Sodium channels
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  • 1Gangadharan V, Kuner R. Pain hypersensitivity mechanisms at a glance[J]. Dis Model Mech,2013,6(4) :889-895.
  • 2Lai J, Hunter JC, Porreca F. The role of voltage-gated sodium channels in neuropathie pain [ J ]. Curt Opin Neurobio1,2003,13 ( 3 ) :291-297. DOI : 10.1016/S0959-4388 (03)00074-6.
  • 3Waxman SG, Zamponi GW. Regulating excitability of peripheral affer- ents : emerging ion channel targets [ J ]. Nat Neurosci, 2014,17 ( 2 ) : 153-163.
  • 4Datta S, Waghray T, Tortes M, et al. Amiodarone decreases heat, cold, and mechanical hyperalgesia in a rat model of neuropathic pain [J]. Anesth Analg,2004,98( 1 ) :178-184.
  • 5Cox JJ, Reimann F, Nicholas AK, et al. An SCN9A channelopathy causes congenital inability to experience pain [ J ]. Nature, 2006,444 (7121) :894-898.
  • 6Tian J, Gu Y, Su D. Effects of intrathecal lidocaine on hyperalgesia and allodynia following chronic constriction injury in rats [ J ]. Eur J Pain ,2009,13(2) :130-137.
  • 7杨文贵,肖锋,季玉红,孙琳琳,孙文健,马兆龙,袁文,赵剑,沈爱国.大鼠脊髓横断性损伤后细胞周期蛋白D3的表达变化[J].中华实验外科杂志,2007,24(12):1573-1574. 被引量:3

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