Correlation between the microbiome and pack burst spoilage of Allium sativum supplemented fermented hot pepper paste.

Gochujang (fermented hot pepper paste) products are well known for their distinct, spicy flavor. However, frequent pack burst spoilage of gochujang products occurs during transportation and storage because of microbial aerogenesis, resulting in considerable economic losses. The present study aimed to prevent pack burst spoilage of gochujang products by supplementing them with garlic ethanol extract. A simulated pack burst experiment revealed that 42.86 % of normal gochujang products were spoiled. Garlic ethanol extract significantly inhibited the growth of Zygosaccharomyces rouxii in gochujang products, with low minimum inhibitory concentration values (12.5-25 mg/mL). Gochujang products supplemented with various concentrations (1 % and 2.5 %) of garlic ethanol extract exhibited marked inhibition of microbial growth, particularly Z. rouxii, and pack burst spoilage. Microbiome analysis revealed that the pack burst samples harbored a high abundance of Z. rouxii. Supplementation of gochujang with 1 % garlic ethanol extract drastically reduced Z. rouxii abundance and prevented pack burst. Moreover, gochujang products supplemented with 1 % garlic ethanol extract exhibited a high hedonic score in the sensory analysis. Based on the results of this study, we concluded that supplementation of gochujang products with 1 % garlic ethanol extract before packaging could be effective in preventing pack burst spoilage of gochujang.

PharmDB-K: Integrated Bio-Pharmacological Network Database for Traditional Korean Medicine.

Despite the growing attention given to Traditional Medicine (TM) worldwide, there is no well-known, publicly available, integrated bio-pharmacological Traditional Korean Medicine (TKM) database for researchers in drug discovery. In this study, we have constructed PharmDB-K, which offers comprehensive information relating to TKM-associated drugs (compound), disease indication, and protein relationships. To explore the underlying molecular interaction of TKM, we integrated fourteen different databases, six Pharmacopoeias, and literature, and established a massive bio-pharmacological network for TKM and experimentally validated some cases predicted from the PharmDB-K analyses. Currently, PharmDB-K contains information about 262 TKMs, 7,815 drugs, 3,721 diseases, 32,373 proteins, and 1,887 side effects. One of the unique sets of information in PharmDB-K includes 400 indicator compounds used for standardization of herbal medicine. Furthermore, we are operating PharmDB-K via phExplorer (a network visualization software) and BioMart (a data federation framework) for convenient search and analysis of the TKM network. Database URL: http://pharmdb-k.org, http://biomart.i-pharm.org.

20-O-ß-d-glucopyranosyl-20(S)-protopanaxadiol, a metabolite of ginseng, inhibits colon cancer growth by targeting TRPC channel-mediated calcium influx.

Abnormal regulation of Ca(2+) mediates tumorigenesis and Ca(2+) channels are reportedly deregulated in cancers, indicating that regulating Ca(2+) signaling in cancer cells is considered as a promising strategy to treat cancer. However, little is known regarding the mechanism by which Ca(2+) affects cancer cell death. Here, we show that 20-O-ß-d-glucopyranosyl-20(S)-protopanaxadiol (20-GPPD), a metabolite of ginseng saponin, causes apoptosis of colon cancer cells through the induction of cytoplasmic Ca(2+). 20-GPPD decreased cell viability, increased annexin V-positive early apoptosis and induced sub-G1 accumulation and nuclear condensation of CT-26 murine colon cancer cells. Although 20-GPPD-induced activation of AMP-activated protein kinase (AMPK) played a key role in the apoptotic death of CT-26 cells, LKB1, a well-known upstream kinase of AMPK, was not involved in this activation. To identify the upstream target of 20-GPPD for activating AMPK, we examined the effect of Ca(2+) on apoptosis of CT-26 cells. A calcium chelator recovered 20-GPPD-induced AMPK phosphorylation and CT-26 cell death. Confocal microscopy showed that 20-GPPD increased Ca(2+) entry into CT-26 cells, whereas a transient receptor potential canonical (TRPC) blocker suppressed Ca(2+) entry. When cells were treated with a TRPC blocker plus an endoplasmic reticulum (ER) calcium blocker, 20-GPPD-induced calcium influx was completely inhibited, suggesting that the ER calcium store, as well as TRPC, was involved. In vivo mouse CT-26 allografts showed that 20-GPPD significantly suppressed tumor growth, volume and weight in a dose-dependent manner. Collectively, 20-GPPD exerts potent anticarcinogenic effects on colon carcinogenesis by increasing Ca(2+) influx, mainly through TRPC channels, and by targeting AMPK.