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Cilostazol suppresses LPS-stimulated maturation of DC2.4 cells
through inhibition of NF-kappaB pathway
Tianhua Chen,1 Zhiliang Li,1 Qiang Fu,1 Linlin Chen,1 Longxing Cao,1
1 2
Weiwei Zhang, Jianxin Diao
1Department of Cardiology, The Affiliated Zhujiang Hospital of Southern Medical
University, Guangzhou, P.R. China
2Symptomatic Laboratory of Traditional Chinese Medical, Southern Medical
University, Guangzhou, P.R. China
Correspondence: Zhiliang Li, Department of Cardiology, Zhujiang Hospital of
Southern Medical University, No.253 Industry Road, Guangzhou, Guangdong
province, P. R. China. E-mail: leedoctor00@163.com
1
Abstract
Cilostazol is a phosphodiesterase-3 inhibitor that functions as a platelet aggregation
inhibitor and is used for treating peripheral artery diseases and ischemic stroke.
Dendritic cells (DCs) play an active role in the immunological processes related to
atherosclerosis. Cilostazol has anti-atherogenic and anti-inflammatory effects,
however, the effects of cilostazol on DC maturation remain unknown. The purpose of
this study was to determine the effects of cilostazol on lipopolysaccharide
(LPS)-induced maturation of DCs. DC2.4 cells were treated with cilostazol for 12 h
and subsequently stimulated with LPS to induce maturation. Cilostazol reduced the
expression of maturation-associated markers induced by LPS, such as CD40, CD86,
and MHCII; improved the endocytotic function; and decreased production of tumor
necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) of these cells. To further
elucidate
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