Inhibitory Action of Tranilast, an Anti-Allergic Drug, on the Release of Cytokines and PGE2 from Human Monocytes-Macrophages

The Japanese Journal of Pharmacology

Akihide Koda¹  Kiyoshi Ichikawa²  Shinji Kikuchi²  Haruo Suzawa² 

[1] Department of Pharmacology, Gifu Pharmaceutical University;Pharmacological Laboratories, Kissei Pharmaceutical Co., Ltd.

关键词: Tranilast;    Transforming growth factor (TGF)-β1;    Interleukin (IL)-1β;    Macrophage;    Collagen synthesis of fibroblast;   

DOI  :  10.1254/jjp.60.85

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(28)Cited-By(68)Tranilast, an anti-allergic drug that inhibits the release of substances such as histamine and prostaglandins from mast cells, has been reported to improve keloids and hypertrophic scars which originate from the abnormal proliferation and excessive collagen accumulation of fibroblasts. It has been considered that various chemical mediators produced by inflammatory cells play important roles in the development of keloids and hypertrophic scars. We therefore studied the effect of tranilast on the release of chemical mediators including transforming growth factor (TGF)-β1, interleukin (IL)-1β and prostaglandin (PG) E2 which are produced by the human monocytes-macrophages, and estimated whether these mediators induce collagen synthesis and cell proliferation of normal skin fibroblasts. Tranilast inhibited the release of TGF-β1, IL-1β and PGE2 from the human monocytes-macrophages. TGF-β1 (25-200 pM) enhanced the collagen synthesis by fibroblasts. IL-1 (0.1-1 U/ml) increased the proliferation and conversely decreased the collagen synthesis. PGE2 (2 μg/ml) enhanced the collagen synthesis. These results suggest that tranilast suppresses collagen synthesis by fibroblasts through inhibiting TGF-β1 and PGE2 production and cell proliferation by fibroblasts through inhibiting IL-1 production by inflammatory cells such as macrophages.

【 授权许可】

Unknown