中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
10期
1185-1188
,共4页
王静捷%陈广俊%陈雯%杜金%罗爱伦%黄宇光
王靜捷%陳廣俊%陳雯%杜金%囉愛倫%黃宇光
왕정첩%진엄준%진문%두금%라애륜%황우광
卡配因%背角细胞%疼痛%炎症%足
卡配因%揹角細胞%疼痛%炎癥%足
잡배인%배각세포%동통%염증%족
Calpain%Dorsal horn cells%Pain%Inflammation%Foot
目的 探讨脊髓背角卡配因在大鼠足底炎性痛形成中的作用.方法 雄性SD大鼠48只,6周龄,体重160~200 g,采用随机数字表法,将其随机分为3组:正常对照组(C组,n=8)、PBS组(n=16)和酵母多糖诱发足底炎性痛组(Z组,n=24).Z组于大鼠左侧后足足底皮下注射酵母多糖1.25 mg,制备酵母多糖诱发足底炎性痛模型,PBS组给予等容量PBS 100μl.分别于给药前(T0)、给药后30 min(T1)、1 h(T2)、2 h(T3)、4 h(T4)、8 h(T5)、24 h(T6)和48 h(T7)时测定左侧后足机械刺激缩足阈值(MWT)、热缩足反应潜伏期(PWTL)和左侧后足足底最大厚度.PBS组于T4时处死8只大鼠,Z组分别于T4、T6和T7时各处死8只大鼠,取左侧脊髓L4~6节段,采用Western blot法测定脊髓背角spectrin αⅡ降解产物、IκBα、环氧化酶-2(COX-2)的表达和NF-κB活性.结果 与C组比较,Z组MWT降低,PWTL缩短,足底最大厚度增厚,脊髓背角spectrin αⅡ降解产物和COX-2的表达上调,IκBα表达下调,NF-κB活性升高(P<0.05或0.01),PBS组上述指标差异无统计学意义(P>0.05).结论 脊髓背角卡配因活化参与了大鼠足底炎性痛的形成,其机制与激活NF-κB,上调COX-2表达有关.
目的 探討脊髓揹角卡配因在大鼠足底炎性痛形成中的作用.方法 雄性SD大鼠48隻,6週齡,體重160~200 g,採用隨機數字錶法,將其隨機分為3組:正常對照組(C組,n=8)、PBS組(n=16)和酵母多糖誘髮足底炎性痛組(Z組,n=24).Z組于大鼠左側後足足底皮下註射酵母多糖1.25 mg,製備酵母多糖誘髮足底炎性痛模型,PBS組給予等容量PBS 100μl.分彆于給藥前(T0)、給藥後30 min(T1)、1 h(T2)、2 h(T3)、4 h(T4)、8 h(T5)、24 h(T6)和48 h(T7)時測定左側後足機械刺激縮足閾值(MWT)、熱縮足反應潛伏期(PWTL)和左側後足足底最大厚度.PBS組于T4時處死8隻大鼠,Z組分彆于T4、T6和T7時各處死8隻大鼠,取左側脊髓L4~6節段,採用Western blot法測定脊髓揹角spectrin αⅡ降解產物、IκBα、環氧化酶-2(COX-2)的錶達和NF-κB活性.結果 與C組比較,Z組MWT降低,PWTL縮短,足底最大厚度增厚,脊髓揹角spectrin αⅡ降解產物和COX-2的錶達上調,IκBα錶達下調,NF-κB活性升高(P<0.05或0.01),PBS組上述指標差異無統計學意義(P>0.05).結論 脊髓揹角卡配因活化參與瞭大鼠足底炎性痛的形成,其機製與激活NF-κB,上調COX-2錶達有關.
목적 탐토척수배각잡배인재대서족저염성통형성중적작용.방법 웅성SD대서48지,6주령,체중160~200 g,채용수궤수자표법,장기수궤분위3조:정상대조조(C조,n=8)、PBS조(n=16)화효모다당유발족저염성통조(Z조,n=24).Z조우대서좌측후족족저피하주사효모다당1.25 mg,제비효모다당유발족저염성통모형,PBS조급여등용량PBS 100μl.분별우급약전(T0)、급약후30 min(T1)、1 h(T2)、2 h(T3)、4 h(T4)、8 h(T5)、24 h(T6)화48 h(T7)시측정좌측후족궤계자격축족역치(MWT)、열축족반응잠복기(PWTL)화좌측후족족저최대후도.PBS조우T4시처사8지대서,Z조분별우T4、T6화T7시각처사8지대서,취좌측척수L4~6절단,채용Western blot법측정척수배각spectrin αⅡ강해산물、IκBα、배양화매-2(COX-2)적표체화NF-κB활성.결과 여C조비교,Z조MWT강저,PWTL축단,족저최대후도증후,척수배각spectrin αⅡ강해산물화COX-2적표체상조,IκBα표체하조,NF-κB활성승고(P<0.05혹0.01),PBS조상술지표차이무통계학의의(P>0.05).결론 척수배각잡배인활화삼여료대서족저염성통적형성,기궤제여격활NF-κB,상조COX-2표체유관.
Objective To investigate the role of calpain in the spinal dorsal horn in development of paw inflammatory pain in rats.Methods Forty-eight male SD rats,aged 6 weeks,weighing 160-200 g,were randomly divided into three groups:normal control group(group C,n =8),PBS group( n =16),zymosan-induced paw inflammatory pain group (group Z,n =24).Inflammatory pain was induced by injection of zymosan 1.25 mg into the plantar surface of left hindpaw.Group PBS received the equal volume of PBS 100 μl.The mechanical paw withdrawal threshold (MWT),paw withdrawal thermal latency (PWTL) and maximum thickness of the plantar surface of left hindpaw were measured before (T0 ) and at 30 min,1,2,4,8,24 and 48 h(T1-7 ) after zymosan or PBS injection.Eight rats were sacrificed at T4 in group PBS and at T4.6,7 in group Z respectively.The left lumbar segment (L4-6) was removed to determination of spectrin α Ⅱ breakdown products,IκBα,cyclooxygenase-2 (COX-2)expression and NF-κB activity in the spinal dorsal horn by Western blot.Results Compared with group C,MWT and PWTL were significantly decreased,maximum thickness of paw and NF-κB activity in the spinal dorsal horn were significantly increased,spectrin α Ⅱ breakdown products and COX-2 expression in the spinal dorsal horn were upregulated,while IκBα expression was down-regulated in group Z( P < 0.05 or 0.01 ),but no significant change was found in group PBS( P > 0.05).Conclusion The activation of calpain in the spinal dorsal horn is involved in the development of paw inflammatory pain in rats through activating NF-κB and up-regulating the expression of COX-2.