Department of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Department of Dermatological Health Management, Eulji University, Seongnam, Korea.
J Ginseng Res. 2015 Jan;39(1):61-8. doi: 10.1016/j.jgr.2014.06.002. Epub 2014 Jun 19.
Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity.
We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models.
PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-α, and prostaglandin E2], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-α, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels.
These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).
高丽参是一种具有多种药理作用的代表性传统草药，包括抗癌、抗动脉粥样硬化、抗糖尿病和抗炎活性。只有少数研究探索了高丽参介导抗炎活性的分子机制。
我们使用体外和体内炎症模型研究了高丽参原人参二醇皂苷（PPD-SF）的抗炎机制。
PPD-SF 呈剂量依赖性地减少炎症介质（一氧化氮（NO）、肿瘤坏死因子-α 和前列腺素 E2）的释放，并下调其相应基因（诱导型一氧化氮合酶、肿瘤坏死因子-α 和环氧化酶-2）的 mRNA 表达，而不改变细胞活力。PPD-SF 介导的这些事件的抑制似乎受到 p38、c-Jun N 末端激酶（JNK）和 TANK（TRAF 家族成员相关 NF-κB 激活剂结合激酶 1（TBK1）的阻断调节，这些激酶与激活转录因子 2（ATF2）和干扰素调节转录因子 3（IRF3）的激活有关。此外，该部分还通过抑制磷酸化 JNK2 水平改善了 HCl/乙醇/-诱导的胃炎。
这些结果强烈表明，PPD-SF 的抗炎作用可能是通过减少 p38、JNK2 和 TANK 结合激酶 1 相关途径及其相应转录因子（ATF2 和 IRF3）的激活来介导的。
