CAJ | 학술논문

目的评价瑞芬太尼诱发切口痛大鼠痛觉过敏时脊髓和背根神经节神经元蛋白激酶Cα相互作用蛋白1(PICK1)表达的变化.方法雄性SD大鼠32只,体重240 ～ 260 g,42～49日龄,采用随机数字表法,将其分为4组(n=8):对照组(C组)、切口痛组(Ⅰ组)、瑞芬太尼组(R组)和瑞芬太尼+切口痛组(R+Ⅰ组).R组和R+Ⅰ组静脉输注瑞芬太尼1.2 μg· kg-1·min-160 min,C组和Ⅰ组静脉输注生理盐水0.12 ml·kg-1·min-1 60 min.R+Ⅰ组与Ⅰ组分别于制备切口痛模型的同时静脉输注瑞芬太尼和生理盐水.分别于生理盐水或瑞芬太尼输注前(T0)、停止输注后2、6、24和48 h(T1-4)时测定机械缩足反应阈(MWT)和热缩足潜伏期(TWL).于T4时测定痛阈结束后处死大鼠,取L4-6节段脊髓和左侧背根神经节,采用实时定量PCR法测定PICK1 mRNA表达水平,采用Western blot法测定PICK1表达水平.结果与C组比较,R组和R+Ⅰ组MWT降低,TWL缩短,脊髓和背根神经节PICK1及其mRNA表达上调,Ⅰ组MWT降低,TWL缩短(P＜0.05),脊髓和背根神经节PICK1及其mRNA的表达差异无统计学意义(P＞0.05);与Ⅰ组比较,R+Ⅰ组MWT降低,TWL缩短,脊髓和背根神经节PICK1及其mRNA表达上调(P＜0.05);与R组比较,R+Ⅰ组MWT降低,TWL缩短(P＜0.05),脊髓和背根神经节PICK1及其mRNA表达差异无统计学意义(P＞0.05).结论瑞芬太尼诱发切口痛大鼠痛觉过敏形成的机制可能与脊髓和背根神经节神经元PICK1表达上调有关.
목적 평개서분태니유발절구통대서통각과민시척수화배근신경절신경원단백격매Cα상호작용단백1(PICK1)표체적변화.방법 웅성SD대서32지,체중240 ～ 260 g,42～49일령,채용수궤수자표법,장기분위4조(n=8):대조조(C조)、절구통조(Ⅰ조)、서분태니조(R조)화서분태니+절구통조(R+Ⅰ조).R조화R+Ⅰ조정맥수주서분태니1.2 μg· kg-1·min-160 min,C조화Ⅰ조정맥수주생리염수0.12 ml·kg-1·min-1 60 min.R+Ⅰ조여Ⅰ조분별우제비절구통모형적동시정맥수주서분태니화생리염수.분별우생리염수혹서분태니수주전(T0)、정지수주후2、6、24화48 h(T1-4)시측정궤계축족반응역(MWT)화열축족잠복기(TWL).우T4시측정통역결속후처사대서,취L4-6절단척수화좌측배근신경절,채용실시정량PCR법측정PICK1 mRNA표체수평,채용Western blot법측정PICK1표체수평.결과 여C조비교,R조화R+Ⅰ조MWT강저,TWL축단,척수화배근신경절PICK1급기mRNA표체상조,Ⅰ조MWT강저,TWL축단(P＜0.05),척수화배근신경절PICK1급기mRNA적표체차이무통계학의의(P＞0.05);여Ⅰ조비교,R+Ⅰ조MWT강저,TWL축단,척수화배근신경절PICK1급기mRNA표체상조(P＜0.05);여R조비교,R+Ⅰ조MWT강저,TWL축단(P＜0.05),척수화배근신경절PICK1급기mRNA표체차이무통계학의의(P＞0.05).결론 서분태니유발절구통대서통각과민형성적궤제가능여척수화배근신경절신경원PICK1표체상조유관.
Objective To evaluate the changes in the expression of protein interacting with Cα kinase 1 (PICK1) in the spinal cord and dorsal root ganglion (DRG) neurons during remifentanil-induced hyperalgesia in rats with incisional pain.Methods Thirty-two male Sprague-Dawley rats, weighing 240-260 g, aged 42-49 days, were randomly divided into 4 groups (n =8 each) using a random number table: control group (group C) , incisional pain group (group Ⅰ) , remifentanil group (group R), and remifentanil + incisional pain group (group R + Ⅰ).In R and R+Ⅰ groups, remifentanil was infused intravenously for 60 min at the rate of 1.2 p,g · kg-1 · min-1.In C and Ⅰ groups, normal saline was infused intravenously for 60 min at the rate of 0.12 ml · kg-1 · min-1.In Ⅰ and R+Ⅰ groups, the model of incisional pain was established, and remifentanil and normal saline were infused intravenously, respectively, at the same time.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before normal saline or remifentanil infusion, and at 2, 6, 24, and 48 h after the end of normal saline or remifentanil infusion (T1-4).The rats were sacrificed after the last measurement of pain threshold.The lumbar segment (L4-6) of the spinal cord and left DRGs were removed for determination of the expression of PICKl mRNA (by quantitative real-time reverse transcriptase-polymerase chain reaction) and PICK1 protein (by Western blot).Results Compared with group C, the MWT was significantly decreased, the TWL was shortened, and the expression of PICK1 protein and mRNA was up-regulated in R and R+Ⅰ groups, and the MWT was significantly decreased, the TWL was shortened (P＜0.05) , and no significant change was found in the expression of PICK1 protein and mRNA in group Ⅰ (P＞0.05).Compared with group Ⅰ, the MWT was significantly decreased, the TWL was shortened, and the expression of PICK1 protein and mRNA was up-regulated in group R+Ⅰ (P＜0.05).Compared with group R, the MWT was significantly decreased, the TWL was shortened (P＜0.05) , and no significant change was found in the expression of PICK1 protein and mRNA in group R+ Ⅰ (P＞0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia may be related to up-regulation of PICK1 expression in the spinal cord and DRG neurons of rats with incisional pain.