Major roles of prostanoid receptors IP and EP(3) in endotoxin-induced enhancement of pain perception.
Major roles of prostanoid receptors IP and EP(3) in endotoxin-induced enhancement of pain perception.
复制标题
前列腺素受体 IP 和 EP(3) 在内毒素诱导的疼痛感知增强中的主要作用。
DOI：
10.1016/s0006-2952(01)00654-2
复制
发表时间：
2001
影响因子：
5.8
通讯作者：
S. Oh‐ishi
中科院分区：
文献类型：
--
作者：
A. Ueno;H. Matsumoto;H. Naraba;Y. Ikeda;F. Ushikubi;T. Matsuoka;S. Narumiya;Y. Sugimoto;A. Ichikawa;S. Oh‐ishi
为了了解前列腺素I(IP)和前列腺素E(EP)受体在痛觉中的作用，我们比较了前列腺素受体(IP、EP1、EP2、EP3或EP4)缺乏的小鼠在脂多糖(LPS)预处理或不加脂多糖(LPS)处理的情况下，醋酸诱导的扭体反应。在没有内毒素预处理的情况下，IP受体缺陷小鼠表现出明显较少的反应，而EP受体亚型中任何一种缺陷的小鼠表现出与野生型小鼠相似的扭体反应。当用脂多糖预处理小鼠24小时以诱导环氧合酶-2表达时，野生型以及EP1、EP2或EP4受体缺陷的小鼠表现出类似的扭体反应增强，而IP和EP3受体缺陷的小鼠扭体次数显著增加。这些结果表明，IP和EP3是介导内毒素引起的小鼠扭体反应增强的主要前列腺素受体，即内毒素增强的炎性痛觉。
To know the roles of prostaglandin I (IP) and prostaglandin E (EP) receptors in pain perception, we compared the acetic acid-induced writhing response in mice deficient in prostaglandin receptors, i.e. IP, EP1,EP2,EP3,or EP4,with or without lipopolysaccharide (LPS) pretreatment. Without LPS pretreatment, IP-receptor deficient mice showed a significantly smaller number of responses, as previously reported, whereas mice deficient in any of the EP-receptor subtypes showed a number of writhings similar to those of wild-type mice. When mice were pretreated with LPS for 24 hr to induce cyclooxygenase-2 expression, the wild-type as well as EP1-, EP2-, or EP4-receptor-deficient mice showed a similar enhanced writhing response, whereas IP- and EP3-receptor-deficient mice had a significantly less enhanced number of writhings. These results indicate that IP and EP3are the major prostaglandin receptors mediating the enhanced acetic acid-induced writhing response in mice pre-exposed to LPS, i.e. in endotoxin-enhanced inflammatory nociception.