中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
7期
793-795
,共3页
周菲%冷玉芳%于洁%吴小精%郝珍%金建萍%胡晓慧%赵文宇
週菲%冷玉芳%于潔%吳小精%郝珍%金建萍%鬍曉慧%趙文宇
주비%랭옥방%우길%오소정%학진%금건평%호효혜%조문우
右美托咪啶%神经痛%JNK丝裂原活化蛋白激酶类%神经节,脊%脊髓
右美託咪啶%神經痛%JNK絲裂原活化蛋白激酶類%神經節,脊%脊髓
우미탁미정%신경통%JNK사렬원활화단백격매류%신경절,척%척수
Dexmedetomidine%Neuropathic pain%JNK mitogen-activated protein kinases%Ganglia,spinal%Spinal cord
目的 评价右美托咪定对神经病理性痛大鼠脊髓背根神经节c-Jun氨基末端激酶(JNK)活化的影响.方法 健康成年雄性SD大鼠54只,体重180 ~ 220 g,采用随机数字表法,将其分为3组(n=18):假手术组(S组)、神经病理性痛组(NP组)和右美托咪定组(D组).采用坐骨神经慢性压迫性损伤法建立大鼠神经病理性痛模型.D组于术后即刻腹腔注射右美托咪定50 μg/kg,1次/d,连续14 d.S组和NP组以等容量生理盐水替代.于术前ld、术后3、7和14 d时测定机械缩足反应阈(MWT)和热缩足反应潜伏期(TWL);于术后3、7和14 d测定痛阈后处死,取损伤侧L4-6脊髓背根神经节,采用免疫组化法测定JNK磷酸化(p-JNK)水平.结果 与S组比较,NP组和D组术后各时点MWT降低,TWL缩短,脊髓背根神经节p-JNK表达上调(P<0.05);与NP组比较,D组术后各时点MWT升高,TWL延长,脊髓背根神经节p-JNK表达下调(P<0.05).结论 右美托咪定减轻大鼠神经病理性痛的机制与抑制脊髓背根神经节JNK活化有关.
目的 評價右美託咪定對神經病理性痛大鼠脊髓揹根神經節c-Jun氨基末耑激酶(JNK)活化的影響.方法 健康成年雄性SD大鼠54隻,體重180 ~ 220 g,採用隨機數字錶法,將其分為3組(n=18):假手術組(S組)、神經病理性痛組(NP組)和右美託咪定組(D組).採用坐骨神經慢性壓迫性損傷法建立大鼠神經病理性痛模型.D組于術後即刻腹腔註射右美託咪定50 μg/kg,1次/d,連續14 d.S組和NP組以等容量生理鹽水替代.于術前ld、術後3、7和14 d時測定機械縮足反應閾(MWT)和熱縮足反應潛伏期(TWL);于術後3、7和14 d測定痛閾後處死,取損傷側L4-6脊髓揹根神經節,採用免疫組化法測定JNK燐痠化(p-JNK)水平.結果 與S組比較,NP組和D組術後各時點MWT降低,TWL縮短,脊髓揹根神經節p-JNK錶達上調(P<0.05);與NP組比較,D組術後各時點MWT升高,TWL延長,脊髓揹根神經節p-JNK錶達下調(P<0.05).結論 右美託咪定減輕大鼠神經病理性痛的機製與抑製脊髓揹根神經節JNK活化有關.
목적 평개우미탁미정대신경병이성통대서척수배근신경절c-Jun안기말단격매(JNK)활화적영향.방법 건강성년웅성SD대서54지,체중180 ~ 220 g,채용수궤수자표법,장기분위3조(n=18):가수술조(S조)、신경병이성통조(NP조)화우미탁미정조(D조).채용좌골신경만성압박성손상법건립대서신경병이성통모형.D조우술후즉각복강주사우미탁미정50 μg/kg,1차/d,련속14 d.S조화NP조이등용량생리염수체대.우술전ld、술후3、7화14 d시측정궤계축족반응역(MWT)화열축족반응잠복기(TWL);우술후3、7화14 d측정통역후처사,취손상측L4-6척수배근신경절,채용면역조화법측정JNK린산화(p-JNK)수평.결과 여S조비교,NP조화D조술후각시점MWT강저,TWL축단,척수배근신경절p-JNK표체상조(P<0.05);여NP조비교,D조술후각시점MWT승고,TWL연장,척수배근신경절p-JNK표체하조(P<0.05).결론 우미탁미정감경대서신경병이성통적궤제여억제척수배근신경절JNK활화유관.
Objective To evaluate the effects of dexmedetomidine on activation of c-Jun N-terminal kinase (JNK) in the dorsal root ganglions of rats with neuropathic pain (NP).Methods Fifty-four male Wistar rats,weighing 180-220 g,were randomly divided into 3 groups with 18 animals in each group using a random number table:sham operation group (group S),NP group and dexmedetomidine group (group D).The animals were anesthetized with intraperitoneal chloral hydrate.NP was induced by chronic constrictive injury.In group S,the right sciatic nerves were only exposed,but not ligated.In group D,dexmedetomidine 50 μg/kg was intraperitoneally injected immediately after operation once a day for 14 consecutive days.In NP and S groups,the rats received the equal volume of normal saline instead of dexmedetomidine.At 1 day before operation (T0) and 3,7 and 14 days after operation (T1-3),mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.The rats in each group were sacrificed after measurement of pain threshold at T1-3 and the ipsilateral dorsal root ganglions of the lumbar segment (L4-6) were removed to detect the phosphorylation of JNK (p-JNK) using immunohistochemistry.Results Compared with group S,MWT was significantly decreased,TWL was shortened,and the expression of p-JNK was up-regulated at each time point after operation in NP and D groups.Compared with group NP,MWT was significantly increased,TWL was prolonged,and the expression of p-JNK was down-regulated at each time point after operation in group D.Conclusion The mechanism by which dexmedetomidine attenuates NP is related to inhibition of activation of JNK in the dorsal root ganglions of rats.