CAJ | 학술논문

目的评价NF-κB信号通路在鞘内注射血小板活化因子(PAF)诱发大鼠痛敏中的作用.方法鞘内置管成功的雄性SD大鼠64只,体重200～250 g,随机分为6组:人工脑脊液(ACSF)对照组(AC组,n=16)鞘内注射ACSF 10μl;PAF诱发大鼠痛敏组(PAF组,n=16)鞘内注射PAF 10μg(溶于10μl ACSF);二甲基亚砜(DMSO)对照组(DC组,n=8)和低、中和高剂量SC-514组(S1-3组,n=8)分别于鞘内注射PAF前2 h腹腔注射0.1%DMSO溶液2 ml、SC-514(溶于2 ml 0.1%DMSO溶液)10、50、100 mg/kg.分别于鞘内给药前、给药后5、15、30、45和60 min时测定机械痛阈和热痛阈,随后每间隔30 min测定1次,连续4 h,ELISA法检测脊髓TNF-α和IL-lβ的表达.结果鞘内注射PAF可诱发机械痛敏和热痛敏,上调大鼠脊髓TNF-α和IL-1β的表达;Iκβ激酶-β抑制剂SC-514可剂量依赖性地减轻PAF诱发的痛敏,抑制脊髓TNF-α和IL-1β的表达上调.结论 NF-κB信号通路参与了鞘内注射PAF诱发大鼠痛敏的过程.
목적 평개NF-κB신호통로재초내주사혈소판활화인자(PAF)유발대서통민중적작용.방법 초내치관성공적웅성SD대서64지,체중200～250 g,수궤분위6조:인공뇌척액(ACSF)대조조(AC조,n=16)초내주사ACSF 10μl;PAF유발대서통민조(PAF조,n=16)초내주사PAF 10μg(용우10μl ACSF);이갑기아풍(DMSO)대조조(DC조,n=8)화저、중화고제량SC-514조(S1-3조,n=8)분별우초내주사PAF전2 h복강주사0.1%DMSO용액2 ml、SC-514(용우2 ml 0.1%DMSO용액)10、50、100 mg/kg.분별우초내급약전、급약후5、15、30、45화60 min시측정궤계통역화열통역,수후매간격30 min측정1차,련속4 h,ELISA법검측척수TNF-α화IL-lβ적표체.결과 초내주사PAF가유발궤계통민화열통민,상조대서척수TNF-α화IL-1β적표체;Iκβ격매-β억제제SC-514가제량의뢰성지감경PAF유발적통민,억제척수TNF-α화IL-1β적표체상조.결론 NF-κB신호통로삼여료초내주사PAF유발대서통민적과정.
Objective To investigate the role of NF-κB pathway in the development of intrathecal(IT)platelet-activating factor (PAF)-induced hyperalgesia in rats. Methods Sixty-four male SD rats (200-250 g) in which intrathecal catheters were successfully implanted without complications were randomly divided into 6 groups:group Ⅰ received artificial cerebro-spinal fluid (ACSF) 10 μl IT (n = 16); group Ⅱ received PAF 10 μg in ACSF 10 μl IT; group Ⅲ received 0.1% DMSO 2 ml intraperitoneally (IP) (n = 8); group Ⅳ, Ⅴ, Ⅵ received IP SC-514 (a selective IKK-β inhibitor) 10, 50, 100 mg/kg in 0.1% DMSO 2 ml respectively at 2 h before IT PAF. Paw withdrawal threshold to mechanical stimulation (PWMT) and paw withdrawal latency to thermal stimuli (PWTL) were measured before (baseline) and at 5, 15, 30, 45, 60 min and then every 30 min for another 4 h after IT administration. The animals were killed after the last pain threshold measurement at 5 h after IT PAF. The lumbar segment (L4-6) of the spinal cord was removed for determination of TNF-α and IL-lβ content (by ELISA).Results lntrathecal PAF induced tactile allodynia and thermal hyperalgesia rapidly, increased the expression of TNF-α and IL-lβ in lumbar spinal cord. Pretreatment with SC-514 attenuated PAF-induced hyperalgesia and inhibited the increase in TNF-α and IL-1β expression in the spinal cord. Conclusion NF-κB is involved in intrathecal PAF-induced hyperalgesia.