THE PIVOTAL ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA IN THE DEVELOPMENT OF INFLAMMATORY HYPERALGESIA
THE PIVOTAL ROLE OF TUMOR-NECROSIS-FACTOR-ALPHA IN THE DEVELOPMENT OF INFLAMMATORY HYPERALGESIA
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DOI：
10.1111/j.1476-5381.1992.tb14503.x
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发表时间：
1992-11-01
影响因子：
7.3
通讯作者：
FERREIRA, SH
中科院分区：
文献类型：
--
作者：
CUNHA, FQ;POOLE, S;FERREIRA, SH
1观察IL-1β、IL-6、IL-8、肿瘤坏死因子α和角叉菜胶对大鼠痛觉过敏的影响。2、IL-6激活IL-1/前列腺素过敏通路，而不激活IL-8/交感神经介导的痛觉过敏通路。3、肿瘤坏死因子α和角叉菜胶能激活这两条通路。4抗血清中和内源性肿瘤坏死因子α，而抗血清中和内源性IL-1β。IL-6和IL-8分别部分抑制这种反应。5中和内源性IL-1β+IL-8或IL-6+IL-8的抗血清可阻断角叉菜胶的反应。6这些结果表明，肿瘤坏死因子α在炎性痛觉过敏的发生中起着早期和关键的作用。7肿瘤坏死因子α、IL-1β、IL-6和IL-8在炎性痛觉过敏的发生中的作用，以及这些细胞因子的产生被类固醇抗炎药物抑制的发现，为这些药物治疗炎性痛敏提供了作用机制。
1 The hyperalgesic activities in rats of interleukin-1beta (IL-1beta), IL-6, IL-8, tumour necrosis factor alpha (TNFalpha) and carrageenin were investigated.2 IL-6 activated the previously delineated IL-1/prostaglandin hyperalgesic pathway but not the IL-8/sympathetic mediated hyperalgesic pathway.3 TNFalpha and carrageenin activated both pathways.4 Antiserum neutralizing endogenous TNFalpha abolished the response to carrageenin whereas antisera neutralizing endogenous IL-1beta, IL-6 and IL-8 each partially inhibited the response.5 The combination of antisera neutralizing endogenous IL-1beta + IL-8 or IL-6 + IL-8 abolished the response to carrageenin.6 These results show that TNFalpha has an early and crucial role in the development of inflammatory hyperaglesia.7 The delineation of the roles of TNFalpha, IL-1beta, IL-6 and IL-8 in the development of inflammatory hyperalgesia taken together with the finding that the production of these cytokines is inhibited by steroidal anti-inflammatory drugs provides a mechanism of action for these drugs in the treatment of inflammatory hyperalgesia.