中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
6期
712-714
,共3页
付红光%杨现会%李晓悦%张璐瑶%董铁立
付紅光%楊現會%李曉悅%張璐瑤%董鐵立
부홍광%양현회%리효열%장로요%동철립
二异丙酚%炎症%疼痛%受体,GABA%受体,N-甲基-D-天冬氨酸
二異丙酚%炎癥%疼痛%受體,GABA%受體,N-甲基-D-天鼕氨痠
이이병분%염증%동통%수체,GABA%수체,N-갑기-D-천동안산
Propofol%Inflammation%Pain%Receptors,GABA%Receptors,N-methyl-D-aspartate
目的 评价异丙酚对炎性痛大鼠海马γ-氨基丁酸A(GABAA)和N-甲基-D-天冬氨酸受体(NMDA)表达的影响.方法 清洁级成年雄性SD大鼠32只,体重180 ~ 220 g,采用随机数字表法分为4组(n=8):对照组(C组)腹腔注射生理盐水和二甲基亚砜(DMSO)0.1 ml/kg;炎性痛组(IP组)腹腔注射生理盐水+ DMSO 0.1 ml/kg,5 min后于左后掌璞处注射福尔马林制备大鼠炎性痛模型;不同剂量异丙酚组(P1.2组)分别腹腔注射异丙酚30、100 mg/kg,5 min后注射福尔马林.于注射福尔马林后1h内观察大鼠痛行为学,计算痛加权评级(PIS)值,随后断头处死大鼠取海马,采用免疫组化法检测GABAA和NMDA受体的表达.结果 与C组比较,IP组和P1.2组大鼠PIS值升高,海马GABAA受体和NMDA受体表达上调(P<0.05);与IP组比较,P1.2组大鼠PIS值降低,海马GABAA受体上调,NMDA受体表达下调(P<0.05);与P1组比较,P2组大鼠PIS值降低,海马GABAA受体上调,NMDA受体表达下调(P<0.05).结论 腹腔注射异丙酚可下调炎性痛大鼠海马NMDA受体表达,抑制了中枢痛敏反应;上调海马GABAA受体表达,加强机体内源性镇痛机制.
目的 評價異丙酚對炎性痛大鼠海馬γ-氨基丁痠A(GABAA)和N-甲基-D-天鼕氨痠受體(NMDA)錶達的影響.方法 清潔級成年雄性SD大鼠32隻,體重180 ~ 220 g,採用隨機數字錶法分為4組(n=8):對照組(C組)腹腔註射生理鹽水和二甲基亞砜(DMSO)0.1 ml/kg;炎性痛組(IP組)腹腔註射生理鹽水+ DMSO 0.1 ml/kg,5 min後于左後掌璞處註射福爾馬林製備大鼠炎性痛模型;不同劑量異丙酚組(P1.2組)分彆腹腔註射異丙酚30、100 mg/kg,5 min後註射福爾馬林.于註射福爾馬林後1h內觀察大鼠痛行為學,計算痛加權評級(PIS)值,隨後斷頭處死大鼠取海馬,採用免疫組化法檢測GABAA和NMDA受體的錶達.結果 與C組比較,IP組和P1.2組大鼠PIS值升高,海馬GABAA受體和NMDA受體錶達上調(P<0.05);與IP組比較,P1.2組大鼠PIS值降低,海馬GABAA受體上調,NMDA受體錶達下調(P<0.05);與P1組比較,P2組大鼠PIS值降低,海馬GABAA受體上調,NMDA受體錶達下調(P<0.05).結論 腹腔註射異丙酚可下調炎性痛大鼠海馬NMDA受體錶達,抑製瞭中樞痛敏反應;上調海馬GABAA受體錶達,加彊機體內源性鎮痛機製.
목적 평개이병분대염성통대서해마γ-안기정산A(GABAA)화N-갑기-D-천동안산수체(NMDA)표체적영향.방법 청길급성년웅성SD대서32지,체중180 ~ 220 g,채용수궤수자표법분위4조(n=8):대조조(C조)복강주사생리염수화이갑기아풍(DMSO)0.1 ml/kg;염성통조(IP조)복강주사생리염수+ DMSO 0.1 ml/kg,5 min후우좌후장박처주사복이마림제비대서염성통모형;불동제량이병분조(P1.2조)분별복강주사이병분30、100 mg/kg,5 min후주사복이마림.우주사복이마림후1h내관찰대서통행위학,계산통가권평급(PIS)치,수후단두처사대서취해마,채용면역조화법검측GABAA화NMDA수체적표체.결과 여C조비교,IP조화P1.2조대서PIS치승고,해마GABAA수체화NMDA수체표체상조(P<0.05);여IP조비교,P1.2조대서PIS치강저,해마GABAA수체상조,NMDA수체표체하조(P<0.05);여P1조비교,P2조대서PIS치강저,해마GABAA수체상조,NMDA수체표체하조(P<0.05).결론 복강주사이병분가하조염성통대서해마NMDA수체표체,억제료중추통민반응;상조해마GABAA수체표체,가강궤체내원성진통궤제.
Objective To evaluate the effects of propofol on the expression of hippocampal γ-aminobutyric acid (GABAA) and NMDA receptor in a rat model of inflammatory pain (IP).Methods A total of 32 female Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 4 groups (n =8 each):control group (group C),group IP,and different doses of propofol groups (P1,2 groups).IP was induced by injection of formalin.In group C,normal saline and dimethyl sulfoxide (DMSO) 0.1 ml/kg were injected intraperitoneally.In group IP,normal saline and DMSO 0.1 ml/kg were injected intraperitoneally,and 5 min later formalin was injected.In P1,2 groups,propofol 30 and 100 mg/kg were intraperitoneally injected,respectively,and 5 min later formalin was injected.The pain behavior of rats was observed within 1 h after injection of formalin and pain intensity scoring (PIS) value was calculated.The animals were sacrificed at 1 h after injection of formalin and the hippocampi were isolated for determination of GABAA and NMDA receptor expression by immunohistochemisty.Results Compared with group C,PIS value was significantly increased,GABAA and NMDA receptor expression was up-regulated in IP and P1.2 groups.Compared with group IP,PIS value was significantly decreased,GABAA receptor expression was up-regulated,and NMDA receptor expression was down-regulated in P1,2 groups.PIS value was significantly lower,GABAA receptor expression was higher,and NMDA receptor expression was lower in group P2 than in group P1.Conclusion Intraperitoneal propofol can down-regulate NMDA receptor expression in hippocampi of rats with IP,thus inhibiting responses to pain sensitivity; intraperitoneal propofol can up-regulate hippocampal GABAA receptor expression,thus enhancing endogenous mechanism of analgesia.