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Title 

5-(4-Hydroxy-2,3,5-trimethylbenzylidene) thiazolidine-2,4-dione attenuates atherosclerosis possibly by reducing monocyte recruitment to the lesion

Authors 

J H ChoiJ G ParkH J JeonM S KimM R LeeM N LeeS K SonnJ H KimM H LeeM S ChoiY B ParkO S KwonTae Sook JeongWoo Song LeeH B ShimD H ShinG T Oh

Publisher 

Korean Society of Medical Biochemistry

Issue Date 

2011

Citation 

Experimental and Molecular Medicine, vol. 43, no. 8, pp. 471-478

Keywords 

AntioxidantsArachidonate 5-lipoxygenaseAtherosclerosisEndothelial cellsMacrophages

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 B4 (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-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.

ISSN 

1226-3613

Link 

http://dx.doi.org/10.3858/emm.2011.43.8.053

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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