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作 者:王静捷[1] 陈雯[1] 黄宇光[1] 罗爱伦[1]
机构地区:[1]中国医学科学院北京协和医学院北京协和医院麻醉科,100730
出 处:《北京医学》2010年第8期644-647,共4页Beijing Medical Journal
摘 要:目的评价该模型大鼠的疼痛行为学特点和炎性水肿程度,并对该模型大鼠脊髓背角COX-2表达水平进行分析。方法 SD大鼠48只,随机分为3组,即对照组(n=8)、假手术组(n=16)及zymosan组(n=24)。按Meller方法制作zymosan足底炎性疼痛模型,假手术组在左侧后足皮下注射同等容积的PBS。采用电子VonFrey压力测痛仪、热板和电子数显卡尺分别于制模后0.5h、1h、2h、4h、8h、24h和48h测定各组大鼠左侧后足机械刺激缩足阈值、热敏缩足反射阈值和左足最大厚度。各组大鼠在指定时间点处死后取制模侧腰段脊髓背角,采用Western blot方法测定脊髓背角中COX-2表达水平。结果与对照组和假手术组比较,zymosan组大鼠制模侧后足机械刺激缩足阈值和热敏缩足反射阈值显著降低(P<0.05,P<0.01),最大厚度显著增加(P<0.01),提示zymosan组大鼠出现机械痛敏、热痛敏和炎性水肿。Zymosan组大鼠制模侧脊髓背角COX-2表达水平显著增加,与对照组和假手术组比较有显著性差异(P<0.05)。结论 Zymosan足底炎性疼痛大鼠模型可以产生持续的、可信的痛觉过敏,与人体损伤后情况基本一致,并诱导脊髓背角COX-2表达水平增加,是研究组织损伤诱发炎性疼痛机制的较佳选择。Objective To establish zymosan-induced paw inflammatory pain model in the rat and characterize the time-dependent mechanical and thermal hyperalgesia and paw edema, meanwhile investigate the COX-2 expression in the spinal dorsal horn.Methods Forty-eight Sprague-Dawley rats were divided into three groups:1) control rats (n=8), 2) sham surgery rats (n=16), 3) zymosan-induced paw inflammation rats (n=24).According to Meller's method, zymosan (1.25mg) or equal volume of PBS were injected intraplantarlly.Mechanical withdrawal threshold, paw withdrawal thermal latency and maximum thickness of paw were tested with von Frey filament, hot plate and calibrated micrometer at 0.5h、1h、2h、4h、8h、24h and 48h after zymosan injection, respectively.All rats were killed at different occasions following surgery to examine COX-2 expression in the spinal dorsal horn with the means of western blot analysis.Results Mechanical withdrawal threshold and paw withdrawal thermal latency in the zymosan-induced paw inflammation rats significantly decreased, while maximum thickness of paw significantly increased, comopared with control and sham rats (P0.05, P0.01).COX-2 expression in the ipsilateral spinal dorsal horn dramatically increased after zymosan intraplantar injection (P0.05).Conclusions Intraplantar zymosan injection produces a reliable model of mechanical and thermal hyperalgesia in the rat and contributes to spinal COX-2 expression up-regulation.
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