中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
12期
1460-1463
,共4页
陈春生%刘玉秋%时飞%刘孝杰
陳春生%劉玉鞦%時飛%劉孝傑
진춘생%류옥추%시비%류효걸
受体,CCR2%丝裂原激活蛋白激酶类%炎症%疼痛%神经节,脊
受體,CCR2%絲裂原激活蛋白激酶類%炎癥%疼痛%神經節,脊
수체,CCR2%사렬원격활단백격매류%염증%동통%신경절,척
Receptors,CCR2%Mitogen-activated protein kinases%Inflammation%Pain%Ganglia,spinal
目的 探讨炎性痛大鼠背根神经节趋化因子受体2(CCR2)与p38丝裂原活化蛋白激酶(p38MAPK)信号通路的关系,进一步明确炎性痛的发生机制.方法 健康雌性SD大鼠72只,体重150 ～ 180 g,3～4月龄,采用随机数字表法分为3组(n=24):对照组(C组)于右后足底注射生理盐水100 μl;炎性痛组(IP组)于右后足底注射完全弗氏佐剂100μl; CCR2抑制剂RS102895组(RS组)于右后足底注射完全弗氏佐剂100μl,同时腹腔注射RS102895 20mg/kg,连续7d,1次/d.于注药前与注药后1、3、5、7d测定右后足底机械缩足反应阈(MWT).于注药后3、5、7d随机取8只大鼠,采用免疫组化法测定背根神经节CCR2与磷酸化p38MAPK (p-p38MAPK)的表达水平,RT-PCR法测定CCR2与p38MAPK的mRNA表达水平.结果 与C组比较,IP组和RS组注药后各时点MWT降低,背根神经节CCR2和p-p38MAPK阳性细胞计数和免疫组化染色评分升高,CCR2和p38MAPK的mRNA表达均上调(P＜0.05);与iP组比较,RS组注药后各时点MWT升高,背根神经节CCR2和p-p38MAPK阳性细胞计数和免疫组化染色评分降低,CCR2和p38MAPK的mRNA表达均下调(P＜0.05).结论 背根神经节CCR2可能通过激活p38MAPK信号通路参与了大鼠炎性痛的发生.
目的 探討炎性痛大鼠揹根神經節趨化因子受體2(CCR2)與p38絲裂原活化蛋白激酶(p38MAPK)信號通路的關繫,進一步明確炎性痛的髮生機製.方法 健康雌性SD大鼠72隻,體重150 ～ 180 g,3～4月齡,採用隨機數字錶法分為3組(n=24):對照組(C組)于右後足底註射生理鹽水100 μl;炎性痛組(IP組)于右後足底註射完全弗氏佐劑100μl; CCR2抑製劑RS102895組(RS組)于右後足底註射完全弗氏佐劑100μl,同時腹腔註射RS102895 20mg/kg,連續7d,1次/d.于註藥前與註藥後1、3、5、7d測定右後足底機械縮足反應閾(MWT).于註藥後3、5、7d隨機取8隻大鼠,採用免疫組化法測定揹根神經節CCR2與燐痠化p38MAPK (p-p38MAPK)的錶達水平,RT-PCR法測定CCR2與p38MAPK的mRNA錶達水平.結果 與C組比較,IP組和RS組註藥後各時點MWT降低,揹根神經節CCR2和p-p38MAPK暘性細胞計數和免疫組化染色評分升高,CCR2和p38MAPK的mRNA錶達均上調(P＜0.05);與iP組比較,RS組註藥後各時點MWT升高,揹根神經節CCR2和p-p38MAPK暘性細胞計數和免疫組化染色評分降低,CCR2和p38MAPK的mRNA錶達均下調(P＜0.05).結論 揹根神經節CCR2可能通過激活p38MAPK信號通路參與瞭大鼠炎性痛的髮生.
목적 탐토염성통대서배근신경절추화인자수체2(CCR2)여p38사렬원활화단백격매(p38MAPK)신호통로적관계,진일보명학염성통적발생궤제.방법 건강자성SD대서72지,체중150 ～ 180 g,3～4월령,채용수궤수자표법분위3조(n=24):대조조(C조)우우후족저주사생리염수100 μl;염성통조(IP조)우우후족저주사완전불씨좌제100μl; CCR2억제제RS102895조(RS조)우우후족저주사완전불씨좌제100μl,동시복강주사RS102895 20mg/kg,련속7d,1차/d.우주약전여주약후1、3、5、7d측정우후족저궤계축족반응역(MWT).우주약후3、5、7d수궤취8지대서,채용면역조화법측정배근신경절CCR2여린산화p38MAPK (p-p38MAPK)적표체수평,RT-PCR법측정CCR2여p38MAPK적mRNA표체수평.결과 여C조비교,IP조화RS조주약후각시점MWT강저,배근신경절CCR2화p-p38MAPK양성세포계수화면역조화염색평분승고,CCR2화p38MAPK적mRNA표체균상조(P＜0.05);여iP조비교,RS조주약후각시점MWT승고,배근신경절CCR2화p-p38MAPK양성세포계수화면역조화염색평분강저,CCR2화p38MAPK적mRNA표체균하조(P＜0.05).결론 배근신경절CCR2가능통과격활p38MAPK신호통로삼여료대서염성통적발생.
Objective To investigate the relationship between C-C chemokinereceptor type 2 (CCR2) and p38 mitogen-activated protein kinase (p38MAPK) signaling pathway in the dorsal root ganglion of rats and further clarify the mechanism of inflammatory pain.Methods Sevemy-two female Sprague-Dawley rats,weighing 150-180 g,aged 3-4 months,were randomly divided into 3 groups (n =24 each) using a random number table:control group (group C),inflammatory pain group (IP group) and CCR2 inhibitor RS102895 group (group RS).Inflammatory pain was induced by subcutaneous injection of Freund's adjuvant 100μl into the plantar surface of the right hindpaw.RS102895 20 mg/kg was injected subcutaneously once a day for 7 consecutive days in addition to Freund's adjuvant in group RS.Mechanical paw withdrawal threshold (MWT) was measured before injection and at 1,3,5 and 7 days after injection.At 3,5 and 7 days after injection,8 rats in each group were sacrificed and the dorsal root ganglions were removed for determination of the expression of CCR2 and phosphor-p38MAPK (p-p38MAPK) (by immuno-histochemical staining),and CCR2 and p38MAPK mRNA (using fluorescent quantitative PCR).Immuno-histochemical staining was scored.Results Compared with group C,MWT was significantly decreased after injection,the number of p-p38MAPK positive neurons and immuno-histochemical staining score were increased,and CCR2 and p38MAPK mRNA expression was up-regulated in IP and RS groups.Compared with group IP,MWT was significantly increased after injection,the number of p-p38MAPK positive neurons and immuno-histochemical staining score were decreased,and CCR2 and p3gMAPK mRNAexpression was down-regulated in RS group.Conclusion CCR2 in the dorsal root ganglion is involved in the development of inflammato pain possibility through activating p38MAPK signaling pathway in rats.
