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5-(4-Hydroxy-2,3,5-trimethylbenzylidene) thiazolidine-2,4-dione attenuates atherosclerosis possibly by reducing monocyte recruitment to the lesion
- Title
- 5-(4-Hydroxy-2,3,5-trimethylbenzylidene) thiazolidine-2,4-dione attenuates atherosclerosis possibly by reducing monocyte recruitment to the lesion
- Authors
- Choi J.-H.; Park J.-G.; Jeon H.J.; Kim M.-S.; Lee M.-R.; Lee M.-N.; Sonn S.; Kim J.-H.; Lee M.H.; Choi M.-S.; Park Y.B.; Kwon O.-S.; Jeong T.-S.; Lee W.S.; Shim H.B.; Shin D.H.; Oh G.T.
- Ewha Authors
- 오구택; 신동해; 심현보; 손성근; 이미니
- SCOPUS Author ID
- 오구택; 신동해; 심현보; 손성근; 이미니
- Issue Date
- 2011
- Journal Title
- Experimental and Molecular Medicine
- ISSN
- 1226-3613
- Citation
- Experimental and Molecular Medicine vol. 43, no. 8, pp. 471 - 478
- Indexed
- SCI; SCIE; SCOPUS; KCI
- Document Type
- Article
- 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 (LTB 4) 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-α) 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-α, 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.
- DOI
- 10.3858/emm.2011.43.8.053
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
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