中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2008年
3期
249-252
,共4页
张颜波%牛敬忠%周卫华%高翠英%李菁锦%吕国蔚
張顏波%牛敬忠%週衛華%高翠英%李菁錦%呂國蔚
장안파%우경충%주위화%고취영%리정금%려국위
蛋白激酶C%膜转位%疼痛
蛋白激酶C%膜轉位%疼痛
단백격매C%막전위%동통
Protein kinase C%Membrane translocation%Pain
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200~250 g,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30 min经PE-10管注射0.9%生理盐水20 μl、cPKCs和nPKCs激动剂PMA 100 ng(生理盐水稀释至20 μl)、PKC抑制剂H-7 200 μg(生理盐水稀释至20 μl),然后分别注入0.9%生理盐水10 μl冲洗PE-10管.各组于给予福尔马林后30、60、120 min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、60 min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30 min时PKCγ膜转位水平升高,PMA组给予福尔马林后30、60 min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、60 min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.
目的 探討cPKCs在大鼠內髒炎性痛形成中的作用.方法 成年Wistar大鼠96隻,體重200~250 g,雌雄不拘.隨機分為4組(n=24):對照組(C組)、生理鹽水組(NS組)、PMA組和H-7組.大鼠蛛網膜下腔置管後,採用直腸粘膜下註射福爾馬林的方法,製備大鼠內髒炎性痛模型.C組不給予任何處理,NS組、PMA組、H-7組分彆于給予福爾馬林前30 min經PE-10管註射0.9%生理鹽水20 μl、cPKCs和nPKCs激動劑PMA 100 ng(生理鹽水稀釋至20 μl)、PKC抑製劑H-7 200 μg(生理鹽水稀釋至20 μl),然後分彆註入0.9%生理鹽水10 μl遲洗PE-10管.各組于給予福爾馬林後30、60、120 min時取8隻大鼠,測定內髒痛評分,然後取脊髓,測定cPKCs膜轉位水平.結果 與NS組比較,給予福爾馬林後30、60 min時PMA組內髒痛評分升高,H-7組內髒痛評分降低(P<0.05或0.01).與C組比較,NS組給予福爾馬林後30 min時PKCγ膜轉位水平升高,PMA組給予福爾馬林後30、60 min時PKCγ膜轉位水平升高(P<0.01).與Ns組比較,給予福爾馬林後30、60 min時PMA組PKCγ膜轉位水平升高,H-7組PKCγ膜轉位水平降低(P<0.05).結論 cPKCs型的PKCγ亞型參與瞭大鼠內髒炎性痛的形成.
목적 탐토cPKCs재대서내장염성통형성중적작용.방법 성년Wistar대서96지,체중200~250 g,자웅불구.수궤분위4조(n=24):대조조(C조)、생리염수조(NS조)、PMA조화H-7조.대서주망막하강치관후,채용직장점막하주사복이마림적방법,제비대서내장염성통모형.C조불급여임하처리,NS조、PMA조、H-7조분별우급여복이마림전30 min경PE-10관주사0.9%생리염수20 μl、cPKCs화nPKCs격동제PMA 100 ng(생리염수희석지20 μl)、PKC억제제H-7 200 μg(생리염수희석지20 μl),연후분별주입0.9%생리염수10 μl충세PE-10관.각조우급여복이마림후30、60、120 min시취8지대서,측정내장통평분,연후취척수,측정cPKCs막전위수평.결과 여NS조비교,급여복이마림후30、60 min시PMA조내장통평분승고,H-7조내장통평분강저(P<0.05혹0.01).여C조비교,NS조급여복이마림후30 min시PKCγ막전위수평승고,PMA조급여복이마림후30、60 min시PKCγ막전위수평승고(P<0.01).여Ns조비교,급여복이마림후30、60 min시PMA조PKCγ막전위수평승고,H-7조PKCγ막전위수평강저(P<0.05).결론 cPKCs형적PKCγ아형삼여료대서내장염성통적형성.
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 Ⅲ PMA(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 20 μl NS) and H-7 200 μg(in 20 μl NS)were injected into the subarachnoid space through the spinal catheter in group Ⅱ,Ⅲ and Ⅳ respectively 30 min before rectal submucosal formalin injection.VIP was assessed at 30(T1),60(T2) and 120 (T3) min 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(L6-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 membroxle translocation at T1 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.