前列腺素E1和E2可抑制脂多糖诱导的单核细胞中白细胞介素-18的产生。
Prostaglandins E1 and E2 inhibit lipopolysaccharide-induced interleukin-18 production in monocytes.
作者信息
Takahashi Hideo K, Iwagaki Hiromi, Mori Shuji, Yoshino Tadashi, Tanaka Noriaki, Nishibori Masahiro
机构信息
Department of Pharmacology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
出版信息
Eur J Pharmacol. 2005 Jul 11;517(3):252-6. doi: 10.1016/j.ejphar.2005.05.020.
The purpose of this present study was to explore the therapeutic potential of prostaglandins E1 and E2 on the systemic inflammatory response evoked by endotoxin. Since interleukin-18, a monocyte-derived cytokine, is increased during sepsis, decreasing the production of interleukin-18 is important in treating this condition. Prostaglandin E1 and E2 inhibited interleukin-18 production in human monocytes treated with lipopolysaccharide and prostanoid IP-, EP2- and EP4-receptor agonists mimicked the effects of prostaglandins E1 and E2. Therefore, prostanoid IP, EP2- and EP4-receptors might be involved in the decrease in interleukin-18 production during sepsis.
本研究的目的是探讨前列腺素E1和E2对内毒素诱发的全身炎症反应的治疗潜力。由于白细胞介素-18（一种单核细胞衍生的细胞因子）在脓毒症期间会增加，减少白细胞介素-18的产生对治疗这种疾病很重要。前列腺素E1和E2抑制脂多糖处理的人单核细胞中白细胞介素-18的产生，前列腺素IP、EP2和EP4受体激动剂模拟了前列腺素E1和E2的作用。因此，前列腺素IP、EP2和EP4受体可能参与了脓毒症期间白细胞介素-18产生的减少。
Zotero 插件