Baek Kwang-Soo, Hong Yong Deog, Kim Yong, Sung Nak Yoon, Yang Sungjae, Lee Kyoung Min, Park Joo Yong, Park Jun Seong, Rho Ho Sik, Shin Song Seok, Cho Jae Youl
Department of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Skin Research Institute, AmorePacific R&D Center, Yongin, Korea.
J Ginseng Res. 2015 Apr;39(2):155-61. doi: 10.1016/j.jgr.2014.10.004. Epub 2014 Nov 8.
Korean ginseng is an ethnopharmacologically valuable herbal plant with various biological properties including anticancer, antiatherosclerosis, antidiabetic, and anti-inflammatory activities. Since there is currently no drug or therapeutic remedy derived from Korean ginseng, we developed a ginsenoside-enriched fraction (AP-SF) for prevention of various inflammatory symptoms.
The anti-inflammatory efficacy of AP-SF was tested under in vitro inflammatory conditions including nitric oxide (NO) production and inflammatory gene expression. The molecular events of inflammatory responses were explored by immunoblot analysis.
AP-SF led to a significant suppression of NO production compared with a conventional Korean ginseng saponin fraction, induced by both lipopolysaccharide and zymosan A. Interestingly, AP-SF strongly downregulated the mRNA levels of genes for inducible NO synthase, tumor necrosis factor-α, and cyclooxygenase) without affecting cell viability. In agreement with these observations, AP-SF blocked the nuclear translocation of c-Jun at 2 h and also reduced phosphorylation of p38, c-Jun N-terminal kinase, and TAK-1, all of which are important for c-Jun translocation.
Our results suggest that AP-SF inhibits activation of c-Jun-dependent inflammatory events. Thus, AP-SF may be useful as a novel anti-inflammatory remedy.
高丽参是一种具有民族药理学价值的草本植物,具有多种生物学特性,包括抗癌、抗动脉粥样硬化、抗糖尿病和抗炎活性。由于目前尚无源自高丽参的药物或治疗方法,我们开发了一种富含人参皂苷的组分(AP-SF)用于预防各种炎症症状。
在体外炎症条件下,包括一氧化氮(NO)产生和炎症基因表达,测试AP-SF的抗炎功效。通过免疫印迹分析探索炎症反应的分子事件。
与传统高丽参皂苷组分相比,AP-SF导致脂多糖和酵母聚糖A诱导的NO产生显著受到抑制。有趣的是,AP-SF强烈下调诱导型NO合酶、肿瘤坏死因子-α和环氧化酶基因的mRNA水平,而不影响细胞活力。与这些观察结果一致,AP-SF在2小时时阻断了c-Jun的核转位,还降低了p38、c-Jun氨基末端激酶和TAK-1的磷酸化,所有这些对于c-Jun转位都很重要。
我们的结果表明,AP-SF抑制c-Jun依赖性炎症事件的激活。因此,AP-SF可能作为一种新型抗炎药物有用。