Choi Han-Seok, Seo Hye Sook, Kim Soon Re, Choi Youn Kyung, Jang Bo-Hyoung, Shin Yong-Cheol, Ko Seong-Gyu
Laboratory of Clinical Biology and Pharmacogenomics and Center for Clinical Research and Genomics, Institute of Oriental Medicine, Kyung Hee University, Seoul, 130‑701, Republic of Korea.
Mol Med Rep. 2014 Jan;9(1):311-5. doi: 10.3892/mmr.2013.1775. Epub 2013 Nov 4.
Inflammatory response is a major defense mechanism against pathogens and chemical or mechanical injury. Rhus verniciflua Stokes (RVS) has traditionally been used as an ingredient in East Asian medicine for the treatment of gastritis, stomach cancer and atherosclerosis. The aim of the current study was to analyze the effect of RVS on LPS‑induced inflammatory responses in the RAW264.7 mouse macrophage cell line. RAW264.7 cells were treated with various concentrations of RVS and LPS at specific time points. WST assay, trypan blue assay and quantification of activated cells revealed that RVS suppressed cell proliferation in a dose‑dependent manner. RVS induced G1 cell cycle arrest, suppressed iNOS and COX‑2 mRNA expression induced by LPS and decreased intracellular ROS levels induced by LPS. In addition, RVS induced PARP and caspase‑3 cleavage suggesting that RVS causes cell death. Results of the present study indicate that RVS may be advantageous in treating inflammatory disease.
炎症反应是抵御病原体以及化学或机械损伤的主要防御机制。漆树(Rhus verniciflua Stokes,RVS)在传统东亚医学中一直被用作治疗胃炎、胃癌和动脉粥样硬化的成分。本研究的目的是分析RVS对RAW264.7小鼠巨噬细胞系中脂多糖(LPS)诱导的炎症反应的影响。在特定时间点用不同浓度的RVS和LPS处理RAW264.7细胞。WST检测、台盼蓝检测和活化细胞定量显示,RVS以剂量依赖性方式抑制细胞增殖。RVS诱导G1期细胞周期阻滞,抑制LPS诱导的诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)mRNA表达,并降低LPS诱导的细胞内活性氧(ROS)水平。此外,RVS诱导聚(ADP-核糖)聚合酶(PARP)和半胱天冬酶-3(caspase-3)裂解,表明RVS导致细胞死亡。本研究结果表明,RVS在治疗炎症性疾病方面可能具有优势。