• Korean Journal of Food Science and Technology
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• v.53 no.3
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• pp.344-347
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• 2021

In this study, the hepatotoxic mechanism of chaparral (Larrea tridentata) was investigated through in vitro experiments that measured cell death, inflammatory cytokine secretion, and intracellular fat accumulation by treating HepG2 hepatocytes with a 70% ethanol extract of chaparral at concentrations ranging from 0.001 to 100 ㎍/mL. Cell death was observed after treatment with chaparral extract at concentrations of 1-100 ㎍/mL (p<0.05). The secretion of the inflammatory cytokines, interleukin-8 and macrophage-colony stimulating factor, and fat accumulation were significantly increased even at a concentration of 0.1 ㎍/mL, which was 10 times lower than the observed concentration resulting in cell death (p<0.05). Hepatitis caused by inflammatory cytokine secretion and fat accumulation was shown to be a form of hepatotoxicity induced by chaparral extract. Hepatitis was expressed at a concentration lower than that causing serious toxicity such as cell death, suggesting that hepatotoxicity, including hepatitis, may be caused by ingestion of low concentrations of chaparral.

• Korean Journal of Food Science and Technology
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• v.36 no.5
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• pp.812-817
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• 2004

Cytotoxic effects of Korean rice-wine (Yakju) made with different processes and ingredients (Korean rice-wines I, II), red wine, white wine, beer, and Japanese rice-wine (Sake) were examined against human cancer lines (DLD-1, HepG2, K562) and mouse cancer lines (EMT6, LLC1). Red wine showed cytotoxic effect on all cancer lines, while Korean rice-wines I, and II showed cytotoxcity on all cancer cells except DLD-1. White wine, beer, and Japanese rice-wine had no or little cytotoxic effect against all cancer cell lines. Concentrate of Korean rice-wine only showed cytotoxic effect against DLD-1. These results suggest Korean rice-wine has strong anti-cancer effects, which are induced by certain rice-wine components.

• Culinary science and hospitality research
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• v.20 no.6
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• pp.115-127
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• 2014

This study was carried out to investigate the effectiveness of the Lycopene cultivar of cherry tomatoes as a functional food and food material by measuring the total polyphenol and flavonoid content, anti-oxidative and anticancer activity. The contents of polyphenol and flavonoid were $12.28{\pm}1.78mg$ and $3.89{\pm}0.54mg$ per one g of dried cherry tomatoes respectively. The anti-oxidative activity of the cherry tomato was verified by measuring ${\alpha}$-${\alpha}$-diphenyl-${\beta}$-picrylhydrazyl (DPPH) radical scavenging activity (DSA), 2,2'-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical scavenging activity (ASA) and ferric reducing antioxidant power (FRAP). 50% of radical scavenging concentrations ($IC_{50}$) of DSA and ASA were $328.64{\pm}4.190{\mu}g/mL$ and $350.61{\pm}3.300{\mu}g/mL$ respectively. FRAP value was $26.92{\pm}0.68{\mu}mol$ $Fe^{2+}/g$. The effects of the cherry tomato extract on the growth of a normal lung cell (Hel299), lung cancer cell (A549), cervical cancer cell (HeLa) and a liver cancer cell (HepG2) were investigated using MTT assay. The cherry tomato extract showed a significantly strong growth inhibition effects against A549 cell and $IC_{50}$ was $375.46{\pm}33.670{\mu}g/mL$. The extract also inhibited growths of HeLa and HepG2 cells weakly. In this study we found that Lycopene cultivar of cherry tomato had anti-oxidative activity and strong inhibition effect against lung cancer cells. These results indicate that the Lycopene cultivar of cherry tomato would be a functional food and food material.

• International Journal of Industrial Entomology and Biomaterials
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• v.7 no.2
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• pp.139-144
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• 2003

Over 350 million people worldwide are chronic carriers of hepatitis B virus (HBV). Chronic viral infections of the liver can progress to cirrhosis, which may ultimately lead to hepatic failure or the development of hepatocellular carcinoma. There are two antiviral drugs on the market approved for clinical management of chronic HBV infections; interferon-alpha and the nucleoside analog lamivudine. However, they showed adverse side-effects. In the rational drug design for such therapies we would like to utilize antiviral drugs that inhibit the HBV replication in the liver. Investigation of natural extracts of silkworm exhibiting antiviral potential was held in the functional HBV polymerase activity and the release of virion particle in the HepG2.2.15 cell lines. HBV-producing transgenic mouse fed with silkworm DNJ molecule was shown as an inhibitor of serum HBV particles. We could represent this DNJ molecule as an antiviral potential complementing conventional therapies after preclinical tests against WHBV-infected animal model, woodchuck.

• The Korean Journal of Food And Nutrition
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• v.27 no.4
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• pp.725-731
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• 2014

This study aims to find the correlation the low-molecule fucoidan for cancer prevention with an accelerated formation of cotinine. In the presence of fucoidan, a nicotine to cotinine coversion was studied in established assay, direct mixture method and Hep-G2 cell line method. Fucoidan of $1{\mu}g/mL$ showed the potential effect for converting nicotine to cotinine in the direct mixture method compared to control. Increase of conversion rate at the treatment of fucoidan is exhibited as 15 times compared to control. In Hep-G2 cell treatment, fucoidan showed the potential activity for converting nicotine to cotinine as 6 times compared to control. Therefore, fucoidan was shown to be effective in the conversion of nicotine into cotinine even though it is not higher content of polyphenol and flavonoid than its of green tea extract.

• The Korean Journal of Food And Nutrition
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• v.25 no.1
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• pp.181-187
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• 2012

Grifola frondosa has been used as an herbal medicine for the treatment of cancer, diabetes mellitus and high blood pressure. In this study, functional polysaccharide was obtained from Grifola frondosa using four different extraction methods: hot water(HwFP), homogenize(HgFP), acid(AcFP), and alkali(AlFP) extraction methods. The effects of these extracts on KB and HepG2 cell lines were then examined for any anti-cancer activity. Alkaline extraction produced a yield of 0.175% and the total sugar content of the extract was 54.97%. We were able to confirm that the polysaccharide extracts from the mushroom produce an anti-cancer effect. The cytotoxicity of AlFP and AcFP against HepG2 cells were 22.86% and 28.88%, respectively, and the cytotoxicity of AlFP against the KB cell lines was 47.76% at a concentration of 1,000 ${\mu}g/m{\ell}$. Therefore, these results suggest that the optimum method for extracting functional polysaccharides from G. frondosa is the alkali extraction method.

• Journal of Life Science
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• v.27 no.11
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• pp.1340-1348
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• 2017

Sanguinarine is a benzophenanthridine alkaloid derived from the roots of Sanguinaria canadensis L., which is used for the purpose of treating various diseases. Although studies of anticancer activities have been performed using various cancer cell lines, the phenomenon of inducing apoptosis in cancer cells by using sanguinarine requires more research. Therefore, this study investigated the anti-cancer activities and related mechanisms of sanguinarine used with Hep3B human hepatocellular carcinoma cells in terms of the regulation of apoptosis. Sanguinarine inhibited the proliferation of Hep3B cells in a concentration-dependent manner, which was associated with the induction of apoptosis. Sanguinarine also increased the activity of caspase-3, which is a typical effector caspase, and the activities of caspase-8 and caspase-9, which are key when initiating extrinsic and intrinsic apoptosis pathways, respectively. In addition, sanguinarine increased the expression of death receptor-related genes and pro-apoptotic BAX, which belongs to the Bcl-2 family, while suppressing the expression of anti-apoptotic Bcl-2. Sanguinarine promoted the truncation of Bid and enhanced the release of cytochrome c from the mitochondria to the cytoplasm due to a loss of mitochondrial membrane potential. Furthermore, the reduction of a survival rate that was induced by sanguinarine and the induction of apoptosis disappeared with the inhibition of artificial caspase activity. Therefore, the results of the study indicated that sanguinarine-induced apoptosis in Hep3B cells involves both extrinsic and intrinsic pathways; such apoptosis is a caspase-dependent phenomenon.

• Archives of Pharmacal Research
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• v.23 no.6
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• pp.605-612
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• 2000

Green tea polyphenols (GTP) have been demonstrated to suppress tumorigenesis in several chemical-induced animal carcinogenesis models, and predicted as promising chemopreventive agents in human. Recent studies of GTP extracts showed the involvement of mitogen-activated protein kinases (MAPKs) in the regulation of Phase II enzymes gene expression and induction of apoptosis. In the current work we compared the biological actions of five green tea catechins: (1) induction of ARE reporter gene, (2) activation of MAP kinases, (3) cytotoxicity in human hepatoma HepG2-C8 cells, and (4) caspase activation in human cervical squamous carcinoma HeLa cells. For the induction of phase IIgene assay, (-)-epigallocatechin-3-gallate (EGCG) and (-)-epicatechin-3-gallate (ECG) potently induced antioxidant response element (ARE)-mediated luciferase activity, with induction observed at 25 $\mu\textrm{m}$with EGCG. The induction of ARE reporter gene appears to be structurally related to the 3-gallate group. Comparing the activation of MAPK by the five polyphenols, only EGCG showed potent activation of all three MAPKs (ERK, JNK and p38) in a dose- and time-dependent manner, whereas EGC activated ERK and p38. In the concentration range of 25 $\mu\textrm{m}$ to 1 mM, EGCG and ECG strongly suppressed HepG2-ARE-C8 cell-growth. To elucidate the mechanisms of green tea polyphenol-induced apoptosis, we measured the activation of an important cell death protein, caspase-3 induced by EGCG, and found that caspase-3 was activated in a dose- and time-dependent manner. Interestingly, the activation of caspase-3 was a relatively late event (peaked at 16 h), whereas activation of MAPKs was much earlier (peaked at 2 h). It is possible, that at low concentrations of EGCG, activation of MAPK leads to ARE-mediated gene expression including phase II detoxifying enzymes. Whereas at higher concentrations of EGCG, sustained activation of MAPKs such as JNK leads to apoptosis. These mechanisms are currently under investigation in our laboratory. As the most abundant catechin in GTP extract, we found that EGCG potently induced ARE-mediated gene expression, activated MAP kinase pathway, stimulated caspase-3 activity, and induced apoptosis. These mechanisms together with others, may contribute to the overall chemopreventive function of EGCG itself as well as the GTP.

• Proceedings of the Korean Society for Food Science of Animal Resources Conference
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• 2004.05a
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• pp.314-317
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• 2004

IGF-I rich fraction 분리는 분만 후 24시간이내에 착유한 젖소 초유를 30kDa과 1kDa Ultrafiltra-tion(UF) membrane을 이용하여 분리하였다. 분리한 IGF-I rich fraction은 sandwich ELISA로 정량한 결과 1mg/ml 각 암세포에 미치는 영향을 실험하였다. 그 결과IGF-I rich fraction $1mg/m{\ell}$의 농도로 처리하였을 때 A-427ce11은 33%, SK-HEP-1 cell은 약 2%, A498 cell은 약 22%의 암세포 성장저해 효과를 보였고 HeLa는 약 5% 이하의 세포 증식 저해율과 WiDr cell은 약 30%의 세포성장 저해율을 나타내었으며, 유일하게 위암 세포주인 SNU 16에 대해서는 $1mg/m{\ell}$과 $100{\mu}g/m{\ell}$ 및 $10{\sim}1{\mu}g/m{\ell}$의 농도에서 약 15%와 10% 및 약 5% 이하의 세포 증식율을 나타내었다.

• Genomics & Informatics
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• v.7 no.2
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• pp.97-106
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• 2009

Epigallocatechin gallate (EGCG), a well-known antioxidant molecule, has been reported to cause hepatotoxicity when used in excess. However, the mechanism underlying EGCG-induced hepatotoxicity is still unclear. To better understand the mode of action of EGCG-induced hepatotoxicity, we examined the effect of EGCG on human hepatic gene expression in HepG2 cells using microarrays. Analyses of microarray data revealed more than 1300 differentially expressed genes with a variety of biological processes. Upregulated genes showed a primary involvement with protein-related biological processes, such as protein synthesis, protein modification, and protein trafficking, while downregulated genes demonstrated a strong association with lipid transport. Genes involved in cellular stress responses were highly upregulated by EGCG treatment, in particular genes involved in endoplasmic reticulum (ER) stress, such as GADD153, GADD34, and ATF3. In addition, changes in genes responsible for cholesterol synthesis and lipid transport were also observed, which explains the high accumulation of EGCG-induced lipids. We also identified other regulatory genes that might aid in clarifying the molecular mechanism underlying EGCG-induced hepatotoxicity.