医学临床研究
醫學臨床研究
의학림상연구
JOURNAL OF CLINICAL RESEARCH
2013年
11期
2114-2117
,共4页
龚琴%彭健泓%廖荣宗%胡兴国%曾因明
龔琴%彭健泓%廖榮宗%鬍興國%曾因明
공금%팽건홍%료영종%호흥국%증인명
疼痛%脊髓%大鼠
疼痛%脊髓%大鼠
동통%척수%대서
Pain%Spinal Cord%Rats
[目的]探讨脊髓γ-氨基丁酸转运体-1(GAT-1)在大鼠慢性背根神经节压迫(CCD)神经病理性疼痛中的作用。[方法]选择雄性SD大鼠72只,随机分为假手术组(A组,n=24)、CCD组(B组,n =24)、鞘内NO-711+CCD组( C组,n =24),三组再按不同时段分为6个亚组( n =4),分别于给药前(T0)、给药后1 h (T1)、4 h(T2)、8 h(T3)、16 h(T4)、24 h(T5)时间点处死大鼠取脊髓腰段进行GAT-1蛋白Western Blot实验。[结果]与假手术组相比,B组T0、T1、T2、T3、T4、T5时间点的GAT-1蛋白含量明显增加( P <0.01),鞘内注射生理盐水后,B组的GAT-1蛋白含量无明显改变( P >0.05);与B组和T0相比,鞘内注射20μg NO-711后T1、T2、T3,C组的GAT-1蛋白含量显著降低( P <0.01),鞘内给药后T4,GAT-1蛋白含量逐渐回升,与B组同一时间点比GAT-1蛋白含量仍明显降低( P <0.05),至给药后 T5 GAT-1蛋白含量回升到正常水平( P >0.05)。[结论]CCD模型大鼠脊髓 GAT-1蛋白表达水平上调,GAT 抑制剂 NO-711能明显抑制CCD模型大鼠脊髓GA T-1蛋白表达水平的上调,但是不能抑制GA T-1蛋白基础表达水平。大鼠脊髓背角GA T-1蛋白表达水平的改变与大鼠CCD神经病理性疼痛的机制可能密切相关。
[目的]探討脊髓γ-氨基丁痠轉運體-1(GAT-1)在大鼠慢性揹根神經節壓迫(CCD)神經病理性疼痛中的作用。[方法]選擇雄性SD大鼠72隻,隨機分為假手術組(A組,n=24)、CCD組(B組,n =24)、鞘內NO-711+CCD組( C組,n =24),三組再按不同時段分為6箇亞組( n =4),分彆于給藥前(T0)、給藥後1 h (T1)、4 h(T2)、8 h(T3)、16 h(T4)、24 h(T5)時間點處死大鼠取脊髓腰段進行GAT-1蛋白Western Blot實驗。[結果]與假手術組相比,B組T0、T1、T2、T3、T4、T5時間點的GAT-1蛋白含量明顯增加( P <0.01),鞘內註射生理鹽水後,B組的GAT-1蛋白含量無明顯改變( P >0.05);與B組和T0相比,鞘內註射20μg NO-711後T1、T2、T3,C組的GAT-1蛋白含量顯著降低( P <0.01),鞘內給藥後T4,GAT-1蛋白含量逐漸迴升,與B組同一時間點比GAT-1蛋白含量仍明顯降低( P <0.05),至給藥後 T5 GAT-1蛋白含量迴升到正常水平( P >0.05)。[結論]CCD模型大鼠脊髓 GAT-1蛋白錶達水平上調,GAT 抑製劑 NO-711能明顯抑製CCD模型大鼠脊髓GA T-1蛋白錶達水平的上調,但是不能抑製GA T-1蛋白基礎錶達水平。大鼠脊髓揹角GA T-1蛋白錶達水平的改變與大鼠CCD神經病理性疼痛的機製可能密切相關。
[목적]탐토척수γ-안기정산전운체-1(GAT-1)재대서만성배근신경절압박(CCD)신경병이성동통중적작용。[방법]선택웅성SD대서72지,수궤분위가수술조(A조,n=24)、CCD조(B조,n =24)、초내NO-711+CCD조( C조,n =24),삼조재안불동시단분위6개아조( n =4),분별우급약전(T0)、급약후1 h (T1)、4 h(T2)、8 h(T3)、16 h(T4)、24 h(T5)시간점처사대서취척수요단진행GAT-1단백Western Blot실험。[결과]여가수술조상비,B조T0、T1、T2、T3、T4、T5시간점적GAT-1단백함량명현증가( P <0.01),초내주사생리염수후,B조적GAT-1단백함량무명현개변( P >0.05);여B조화T0상비,초내주사20μg NO-711후T1、T2、T3,C조적GAT-1단백함량현저강저( P <0.01),초내급약후T4,GAT-1단백함량축점회승,여B조동일시간점비GAT-1단백함량잉명현강저( P <0.05),지급약후 T5 GAT-1단백함량회승도정상수평( P >0.05)。[결론]CCD모형대서척수 GAT-1단백표체수평상조,GAT 억제제 NO-711능명현억제CCD모형대서척수GA T-1단백표체수평적상조,단시불능억제GA T-1단백기출표체수평。대서척수배각GA T-1단백표체수평적개변여대서CCD신경병이성동통적궤제가능밀절상관。
[Objective] To explore the role of gamma-aminobutyric acid tranporter-1(GAT-1) in neuro-pathic pain caused by chronic compression of dorsal root ganglion(CCD) in rats .[Methods]A total of 72 male SD rats were randomly divided into sham group(group A ,n=24) ,CCD group(group B ,n=24) and intrathe-cal NO-711+CCD group(group C ,n =24) .According to different time ,three groups were divided into six sub-groups( n=4) .All rats were sacrificed before administration (T0 ) ,1h(T1 ) ,4h(T2 ) ,8h(T3 ) ,16h(T4 ) and 24h(T5 ) after administration .Lumbar spinal cord of rats was collected for Western Blot test of GAT-1 protein .[Results] Compared with sham group ,GAT-1 protein in group B at T0 ,T1 ,T2 ,T3 ,T4 and T5 were obviously increased( P<0 .01) .After intrathecal injection of normal saline ,GAT-1 protein in group B had no obvious change( P>0 .05) .Compared with group B and T0 ,GAT-1 protein in group C at T1 ,T2 and T3 after intrathecal injection with 20 μg NO-711 were markedly decreased ( P <0 .01) .GAT-1 protein was gradually increased at T4 after intrathecal administration .Compared with group B ,GAT-1 protein in group C was still obviously decreased at the same time point( P <0 .05) .GAT-1 protein returned to the normal level until T5 after administration( P>0 .05) .[Conclusion] The expression levels of GAT-1 protein in rat model with CCD are increased .GAT inhibitor NO-711 can obviously inhibit the up-regulation of GAT-1 protein in spine cord of rat model with CCD ,but not inhibit the basic expression level of GAT-1 .The change of GAT-1 protein of spi-nal dorsal horn in rats may be closely correlated with the mechanism of nruropathic pain in rats with CCD .