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作 者:朱亚梅[1] 周玲玲[1] 彭孝武[1] 唐宗湘[1] 周学平[1]
机构地区:[1]南京中医药大学第一临床医学院,江苏南京210023
出 处:《南京中医药大学学报》2016年第3期250-254,共5页Journal of Nanjing University of Traditional Chinese Medicine
基 金:国家自然科学基金(81573869);南京中医药大学国家基金预研基金项目(14XYY01;14XYY10);江苏省普通高校研究生科研创新计划(SJZZ-0122)
摘 要:目的观察清络通痹方对疼痛模型和胶原关节炎(CIA)小鼠模型的疼痛行为的影响,及背根神经节(DRG)环氧合酶(COX)-2mRNA及血前列腺素E2(PGE2)含量的影响,初步探讨清络通痹方干预类风湿关节炎疼痛的作用及可能机制。方法采用热板和醋酸扭体致痛模型,分为空白对照组、塞来昔布组(30mg/kg)、清络通痹低剂量组(4.35g/kg)、中剂量组(8.70g/kg)、高剂量组(17.4g/kg),观察各组痛阈值和扭体次数的改变。DBA/1小鼠,复制CIA模型,随机分为空白对照组、模型组、清络通痹方组(8.7g/kg)及塞来昔布组(30mg/kg),观察一般情况及关节肿胀,各组机械缩足反射阈值(MWT)和热缩足反射阈值(TWL)的变化,灌胃给药4周后,检测DRG COX-2mRNA及血清PGE2含量。结果清络通痹方使小鼠热板法致痛模型痛阈值提高、醋酸扭体法致痛模型扭体次数减少(P<0.01);可显著减轻CIA小鼠足肿胀(P<0.05),提高其MWT(P<0.01)和PWL(P<0.05)阈值,降低DRG中COX-2mRNA的表达(P<0.05)和血PGE2的含量(P<0.05)。结论清络通痹方具有一定的镇痛作用,其镇痛机制可能与抑制DRG中COX-2mRNA表达和血清中PGE2含量相关。OBJECTIVE To study the effects of Qingluo Tongbi Compound(QLT)on pain behavior and COX-2mRNA expression in dorsal root ganglion(DRG)and blood PGE2 concentration,and to explore the mechanisms of pain in rheumatoid arthritis.METHODS The mice were randomly divided into control group,celecoxib 30mg/kg,QLT 4.35g/kg,QLT 8.70g/kg and QLT 17.4g/kg groups.The mice pain threshold change were measured by hot plate method,and body torsion times were tested by acetic acid twisting method.The collagen-induced arthritis(CIA)was induced by collagenⅡ in DBA/1 mice.The mice were randomly divided into control group,CIA group,celecoxib 30mg/kg group,QLT 8.70g/kg.The paws swelling,mechanical withdrawal threshold(MWT)and thermal withdrawal latency(TWL)were recorded.After treated with corresponding drugs by intragastric administration for four weeks,COX-2mRNA in DRG and PGE2 in mice were quantified.RESULTSQLT reduced pain threshold and body torsion times in pain model mice(P〈0.01);compared with the CIA group,the QLT group decreased the paws swelling(P〈0.05),up-regulated MWT(P〈0.01)and PWL(P〈0.05),down-regulated the expression level of COX-2mRNA in DRG and PGE2 concentrations in blood.CONCLUSION QLT shows certain analgesic action,which might be related to the inhibitory effect of COX-2mRNA expression in DRG and PGE2 in blood.
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