摘要
目的:建立免疫复合物致痛模型并与甲醛致炎性痛模型比较,观察大鼠疼痛行为、局部炎症反应及p38 MAPK在脊髓表达的改变,探讨免疫复合物所致疼痛与普通炎性介质致痛的不同特点及发病机制。方法:成年SD健康大鼠30只,随机分为正常对照组、甲醛组及免疫复合物组,每组10只。每组中各取5只大鼠分别鞘内注射DMSO(对照组)或p38 MAPK抑制剂SB203580。各组分别在大鼠右后足底皮下注入20μL PBS、甲醛及免疫复合物,于30 min、1 h、2 h、4 h、8 h、12 h测定疼痛行为,并于12 h后取大鼠脊髓采用Western blotting测定p38及活化p-p38蛋白表达。结果:(1)致痛模型比较:甲醛致痛后大鼠后足立即出现红肿及自发痛,疼痛阈值30 min内迅速下降之后随时间推移缓解,脊髓活化的p-p38表达增加。免疫复合物组大鼠注射部位无红肿表现,疼痛阈值缓慢下降,至注射后8 h达到低谷,脊髓p38无明显活化。(2)p38 MAPK抑制剂SB203580可使甲醛组大鼠局部炎症反应及疼痛阈值下降,但对免疫复合物组及对照组大鼠无效。结论:p38 MAPK活化参与了甲醛所致炎症性疼痛的机制,但不参与免疫复合物致痛机制。本实验建立的抗体复合物致痛模型表现出与甲醛炎性痛不同的疼痛特点。
AIM： To investigate the difference between immune-related pain induced by antigen-special complex and inflammatory pain induced by formalin,and to observe the differential expression of p38 mitogen-activated protein kinase in spinal cord.METHODS： Thirty adult health SD rats were randomly divided into control group,formalin group and immune complex group（10 rats in each group）.After the baseline tests were finished,5 rats in each group underwent intrathecal administration of p38 MAPK inhibitor SB203580.The right hindpaw of the rats were injected with PBS,formalin or rat IgG immune complex.The thickness of hindpaw and pain behaviors were observed at time points of 0 min,30 min,1 h,2 h,4 h,8 h and 12 h after injection.The expression levels of total and activated p38 MAPK in spinal cord were determined by Western blotting analysis.RESULTS： The rats in formalin group showed significant nociceptive behaviors immediately,such as licking foot,and limping with highly swollen foot which could touch the ground.The pain threshold was decreased rapidly 30 min after injection and alleviated after then.The pain threshold of the rats in immune complex group obviously decreased 4 h after injection without red swollen hindpaw.The expression of activated p-p38 MAPK in spinal cord in formalin group was significantly higher than that in immune complex group and control group（P0.01）.No statistic difference of p-p38 expression between immune complex group and control group,also no significant effects of SB203580 on pain behaviors in immune complex group were observed.CONCLUSION： Activated p38 MAPK contributes to the pathogenesis of inflammatory pain,but not to the pathogenesis of immune-related pain.The mechanism of immune-related pain is different from inflammatory pain induced by formalin.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2012年第1期114-117,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.30960473/H2706)
