cPKCs在大鼠内脏炎性痛形成中的作用  

The role of cPKCs in visceral inflammatory pain in rats

作　　者：张颜波[1] 牛敬忠[1] 周卫华[2] 高翠英[3] 李菁锦[3] 吕国蔚[3] 

机构地区：[1]泰山医学院附属医院神经内科,山东省泰安市271000 [2]吉首大学医学院生化教研室 [3]首都医科大学神经生物学系

出　　处：《中华麻醉学杂志》2008年第3期249-252,共4页Chinese Journal of Anesthesiology

摘　　要：目的 探讨cPKCs在大鼠内脏炎性痛形成中的作用。方法 成年Wistar大鼠96只，体重200～250g，雌雄不拘。随机分为4组（n=24）：对照组（C组）、生理盐水组（NS组）、PMA组和H-7组。大鼠蛛网膜下腔置管后，采用直肠粘膜下注射福尔马林的方法，制备大鼠内脏炎性痛模型。C组不给予任何处理，NS组、PMA组、H-7组分别于给予福尔马林前30min经PE-10管注射0．9％生理盐水20μl、cPKCs和nPKCs激动剂PMA 100ng（生理盐水稀释至20μl）、PKC抑制剂H-7200μg（生理盐水稀释至20μl），然后分别注入0．9％生理盐水10出冲洗PE-10管。各组于给予福尔马林后30、60、120min时取8只大鼠，测定内脏痛评分，然后取脊髓，测定cPKCs膜转位水平。结果 与NS组比较，给予福尔马林后30、60min时PMA组内脏痛评分升高，H-7组内脏痛评分降低（P〈0．05或0．01）。与C组比较，NS组给予福尔马林后30min时PKCγ膜转位水平升高，PMA组给予福尔马林后30、60min时PKCγ膜转位水平升高（P〈0．01）。与NS组比较，给予福尔马林后30、60min时PMA组PKCγ膜转位水平升高，H-7组PKCγ膜转位水平降低（P〈0．05）。结论 cPKCs型的PKCγ亚型参与了大鼠内脏炎性痛的形成。Objective To investigate the role of cPKCs in visceral inflammatory pain in rats. Methods Ninety-six adult Wistar rats of both sexes weighing 200-250 g were randomly divided into 4 groups （ n = 24 each） ： group Ⅰ control （C）; group Ⅱ normal saline （NS）; group ⅢPMA （nPKCs and cPKCs agonist） and group IV H-7 （PKC antagonist）. The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. A PE-10 catheter was placed in the subarachnoid space with the tip at lumbar region. Visceral inflammatory pain （VIP） was induced by injecting 5 % formalin 100 μl underneath the mucous membrane of rection. The control group received nothing via spinal catheter. Normal saline 20 μl, PMA 100 ng （in 20μl NS） and H-7 200 μg （in 20 tA NS） were injected into the subarachnoid space through the spinal catheter in group Ⅱ , Ⅲ and Ⅳ respectively 30 rain before rectal submucosal formalin injection. VIP was assessed at 30 （%）, 60 （T2 ） and 120 （T3 ） rain after formalin injection by a numerical scoring system according to Zhang （the higher the number the severer the pain）. Eight animals in each group were killed at the 3 time points after pain behavior assessment, and the lumbar region of the spinal cord （I6-S1-2） for determination of the level of spinal cord cPKCs membrane translocation. Results The pain scores at T1 and T2 were significantly higher in PMA group and lower in H-7 group than in NS group. The levels of PKCγ membrane translocation at Tt and T2 were significantly higher in PMA group and lower in H-7 group than in NS group. Conclusion PKCγ subtype of cPKCs may be involved in the mechanism of visceral inflammatory pain.

关 键 词：蛋白激酶C 膜转位 疼痛 

分 类 号：R285.5[医药卫生—中药学]