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Pristimerin Inhibits Inducible Nitric Oxide Synthase Expression Induced by TLR Agonists
Biomed Sci Letters 2019;25:60-65
Published online March 31, 2019;  https://doi.org/10.15616/BSL.2019.25.1.60
© 2019 The Korean Society For Biomedical Laboratory Sciences.

Su-Yeon Kim* , Sung-Hye Heo* , Sin-Aye Park** and Hyung-Sun Youn,**

Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University, Chungnam, Asan 31538, Korea
Correspondence to: Hyung-Sun Youn. Department of Biomedical Laboratory Science, College of Medical Sciences, Soonchunhyang University, Soonchunhyang-Ro 22, Shinchang-Myun, Asan-Si, Chungnam 31538, Korea.
Tel: +82-41-530-3086, Fax: +82-41-530-3085, e-mail: hyoun@sch.ac.kr
Received January 14, 2019; Accepted March 14, 2019.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
 Abstract
Toll-like receptors (TLRs) are one of the families of pattern recognition receptors (PRR) operating in the innate immunity. TLRs have the ability to recognize relatively conserved microbial components, which are generally referred to as pathogen-associated molecular patterns (PAMPs). The activation of TLRs signaling leads to the activation of NF-觀B and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of pristimerin, which is a naturally occurring triterpenoid compound from Celastraceae plants, iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist), Poly[I:C] (TLR3 agonist), or LPS (TLR4 agonist) were examined. Pristimerin suppressed the iNOS expression induced by MALP-2, Poly[I:C], or LPS. These results suggest that pristimerin can modulate TLRs signaling pathways leading to decreased inflammatory gene expression.
Keywords : Pristimerin; Inducible nitric oxide synthase; TLR; Inflammation; LPS