5-(4-Hyd roxy-2,3,5-tri methylbenzylidene) thiazolidine-2,4-dione attenuates atherosclerosis possibly by reducing monocyte recruitment to the lesionopen access
- Authors
- Choi, Jae-Hoon; Park, Jong-Gil; Jeon, Hyung Jun; Kim, Mi-Sun; Lee, Mi-Ran; Lee, Mi-Ni; Sonn, SeongKeun; Kim, Jae-Hong; Lee, Mun Han; Choi, Myung-Sook; Park, Yong Bok; Kwon, Oh-Seung; Jeong, Tae-Sook; Lee, Woo Song; Shim, Hyun Bo; Shin, Dong Hae; Oh, Goo Taeg
- Issue Date
- Aug-2011
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- antioxidants; arachidonate 5-lipoxygenase; atherosclerosis; endothelial cells; macrophages
- Citation
- EXPERIMENTAL AND MOLECULAR MEDICINE, v.43, no.8, pp.471 - 478
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- EXPERIMENTAL AND MOLECULAR MEDICINE
- Volume
- 43
- Number
- 8
- Start Page
- 471
- End Page
- 478
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/167909
- DOI
- 10.3858/emm.2011.43.8.053
- ISSN
- 1226-3613
- Abstract
- A variety of benzylidenethiazole analogs have been demonstrated to inhibit 5-lipoxygenase (5-LOX). Here we report the anti-atherogenic potential of 5-(4-hydroxy-2,3,5-trimethylbenzylidene) thiazolidin-2,4-dione (HMB-TZD), a benzylidenethiazole analog, and its potential mechanism of action in LDL receptor-deficient (Ldlr(-/-)) mice. HMB-TZD Treatment reduced leukotriene B-4 (LTB4) production significantly in RAW264.7 macrophages and SVEC4-10 endothelial cells. Macrophages or endothelial cells pre-incubated with HMB-TZD for 2 h and then stimulated with lipopolysaccharide or tumor necrosis factor-alpha (TNF-alpha) displayed reduced cytokine production. Also, HMB-TZD reduced cell migration and adhesion in accordance with decreased proinflammatory molecule production in vitro and ex vivo. HMB-TZD treatment of 8-week-old male Ldlr(-/-) mice resulted in significantly reduced atherosclerotic lesions without a change to plasma lipid profiles. Moreover, aortic expression of pro-atherogenic molecules involved in the recruitment of monocytes to the aortic wall, including TNF-alpha, MCP-1, and VCAM-1, was downregulated. HMB-TZD also reduced macrophage infiltration into atherosclerotic lesions. In conclusion, HMB-TZD ameliorates atherosclerotic lesion formation possibly by reducing the expression of proinflammatory molecules and monocyte/macrophage recruitment to the lesion. These results suggest that HMB-TZD, and benzylidenethiazole analogs in general, may have therapeutic potential as treatments for atherosclerosis.
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