Inhibition of LPS-Induced iNOS, COX-2 and Inflammatory Mediator Expression by Paeonol through the MAPKs Inactivation in RAW 264.7 Cells

被引:60
作者
Chae, Hee-Sung [1 ]
Kang, Ok-Hwa [1 ]
Lee, Young-Seob [1 ]
Choi, Jang-Gi [1 ]
Oh, You-Chang [1 ]
Jang, Hye-Jin [1 ]
Kim, Min-San [1 ]
Kim, Jong-Hak [1 ]
Jeong, Seung-Il [2 ]
Kwon, Dong-Yeul [1 ]
机构
[1] Wonkwang Univ, Coll Pharm, Dept Oriental Pharm, Wonkwang Oriental Med Res Inst, Iksan 570749, Chonbuk, South Korea
[2] Jeonju Biomat Inst, Jeonju, Chonbuk, South Korea
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2009年 / 37卷 / 01期
关键词
Paeonol; IL-6; NO; PGE(2); ERK; NITRIC-OXIDE SYNTHASE; MICE; PAIN; CYCLOOXYGENASE-2;
D O I
10.1142/S0192415X0900676X
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
We evaluated the in vivo anti-inflammatory and analgesic activities of orally administered paeonol in mice, and also investigated the anti-inflammatory activity of paeonol in a cell line. Paeonol significantly reduced the edema induced by arachidonic acid in rats. The analgesic effects were assayed using 2 different models, i.e., by acetic acid-induced writhing response and by formalin induced licking and biting time. Moreover, we examined the effects of paeonol on the release of inflammatory mediators such as NO, PGE2 and IL-6. Our results demonstrated that paeonol inhibited LPS induced expression of NO, PGE2 and IL-6. Paeonol prevented LPS induced iNOS, COX-2 and ERK activation. Therefore, paeonol appears to have potential as a treatment for inflammatory disease and analgesic.
引用
收藏
页码:181 / 194
页数:14
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