Abstract: Background: Identifying suitable sites for growing mountain-cultivated ginseng are an area of concern for ginseng producers. This study was conducted to evaluate the soil properties of cultivation sites for mountain-cultivated ginseng in Hamyang-gun, which is known to be one of the most famous areas for mountain-cultivated ginseng in Korea.Methods: The sampling plots from 30 sites were randomly selected on or near the center of the ginseng growing sites in July and August 2009. Soil samples for the soil property analysis were collected through the top 20 cm at five randomly selected points.Results: Mountain-cultivated ginseng was grown in soils that varied greatly in soil properties on coniferous, mixed, and deciduous broadleaved stand sites of elevations between > 200 m and < 1,000 m. The soil bulk density was higher in Pinus densiflora than in Larix leptolepis stand sites and higher in the 700 m sites. Soil pH was unaffected by the type of stand sites (pH 4.35–4.55), while the high-elevation sites of > 700 m were strongly acidified, with pH 4.19. The organic carbon and total nitrogen content were lower in the P. densiflora stand sites than in the deciduous broadleaved stand sites. Available phosphorus was low in all of the stand sites. The exchangeable cation was generally higher in the mixed and low-elevation sites than in the P. densiflora and high-elevation sites, respectively.Conclusion: These results indicate that mountain-cultivated ginseng in Korea is able to grow in very acidic, nutrient-depleted forest soils.

Abstract: Background: Ginsenoside Rp1 (G-Rp1) is a novel ginsenoside derived from ginsenoside Rk1. This compound was reported to have anti-cancer, anti-platelet, and anti-inflammatory activities. In this study, we examined the molecular target of G-Rp1’s anti-proliferative and pro-apoptotic activities.Methods: To examine the effects of G-Rp1, cell proliferation assays, propidium iodine staining, proteomic analysis by two-dimensional gel electrophoresis, immunoblotting analysis, and a knockdown strategy were employed.Results: G-Rp1 dose-dependently suppressed the proliferation of colorectal cancer LoVo cells and also increased the apoptosis of these cells. Interestingly, G-Rp1 remarkably up-regulated the protein level of apolipoprotein (Apo)-A1 in LoVo, SNU-407, DLD-1, SNU-638, AGS, KPL-4, and SK-BR-3 cells. The knockdown of Apo-A1 by its siRNA increased the levels of cleaved poly(ADP-ribose) polymerase (c-PARP) and p53 and diminished the proliferation of LoVo cells.Conclusion: These results suggest that G-Rp1 may act as an anti-cancer agent by strongly inhibiting cell proliferation and enhancing cell apoptosis through the up-regulation of Apo-A1.

Abstract: Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anti-cancer, anti-atherosclerosis, anti-diabetic, and anti-inflammatory activities. Since only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activities, in this study we aimed to investigate 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 (TNF)-α, and prostaglandin E2 (PGE2)], and downregulated the mRNA expression of their corresponding genes [inducible NO synthase (iNOS), TNF-α, and cyclooxygenase (COX)-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-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 EtOH/HCl-induced gastritis via suppression of phospho-JNK2 levels. Therefore, 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 TBK1-linked pathways and their corresponding transcription factors (ATF2/IRF3).