• The Korean Journal of Mycology
• /
• v.36 no.1
• /
• pp.66-74
• /
• 2008

Tremella aurantialba, one of edible and medicinal mushrooms belonging to Tremellaceae of Basidiomycota, has been known to have outstanding curing effects on coughing, tracheitis and hypertension of humans and antitumor activity on the sarcoma 180 and Erhrlich carcinoma of mice. Neutral saline soluble (0.9% NaCl), hot water soluble and methanol soluble substances (hereinafter referred to Fr. NaCl, Fr. HW and Fr. MeOH, respectively) were extracted from fruiting body of the mushroom. In vitro cytotoxicity tests showed that all crude polysaccharides extracted from the fruiting body were not cytotoxic against cancer cell lines such as RAW 309 CR.1 and Sarcoma 180 at the concentration of $2000\;{\mu}g/ml$. Intraperitoneal injection with crude polysaccharides exhibited life prolongation effect of $11.1{\sim}66.7%$ in mice inoculated with Sarcoma 180. Fr. MeOH improved the immunopotentiation activity of B lymphocyte by increasing the alkaline phosphatase activity by 1.16 folds at the concentration of $200\;{\mu}g/ml$. In case of Fr. HW, the numbers of peritoneal exudate cells and circulating leukocytes were increased by 1.42 and 2.87 folds, respectively.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.38 no.2
• /
• pp.142-145
• /
• 2009

The cytotoxic activity against human cancer cells and anti-tumor effect in Balb/c mice of a 70% ethanol extract from masou salmon (MSE) was investigated. The cancer cell lines including human breast adenocarcinoma (MCF-7), human lung carcinoma (A549), human hepatoblastoma (HepG2), human gastric carcinoma (AGS), human cervical adenocarcinoma (HeLa) and transformed primary human embryonal kidney (293) exposed to MSE decreased cell viability as indicated by the MTT assay. The MSE shows significant cytotoxicity on MCF-7, A549, HepG2, AGS and HeLa cells, and are more active than 293 cells. The treatment with 1 mg/mL MSE resulted in 9.2%, 12.7%, 16.6%, and 16.9% cell survival against A549, MCF-7, HepG2, and AGS cells, respectively. Moreover, anticancer effect in vivo of MSE was tested in the animal system using Balb/c mice transplanted sarcoma-180 cells. MSE showed inhibition of tumor growth and the rate of inhibition was 44.7% and 55.7% at the 25 mg/kg body weight and 250 mg/kg body weight, respectively. Thus, we suggest that MSE could be a beneficial material for human cancer prevention.

• The Journal of Internal Korean Medicine
• /
• v.30 no.4
• /
• pp.845-857
• /
• 2009

Background and Objectives : Korean mistletoe lectin (Viscum album coloratum agglutinin, VCA) and bee venom (BV) have been reported to induce apoptosis in various cancer cell lines in vitro and to show antitumor activity against a variety of tumors in animal models. However, the comparative effect of VCA and BV on the anti-cancer effect and mechanisms of action has not been determined. In this study, the effect in a human hepatocellular carcinoma cell line, Hep G2 cells, was examined. Methods : Cytotoxic effects of VCA and BV on Hep G2 cells were determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay in litro. The apoptotic cell death was then confirmed by propidium iodide staining and DNA fragmentation analysis. The mechanisms of action were examined by the expression of anti-apoptotic proteins and activation of mitogen-activated protein kinases. The involvement of kinase was examined in VCA or BV-induced apoptosis by using kinase inhibitors. Results : VCA and BV killed Hep G2 cells in a time and dose-dependent manner. Treatment of Hep G2 cells with VCA activated poly (ADP-ribose) polymerase-1 (PARP-1) known as a marker of apoptosis, and mitogen-activated protein kinases signaling pathways including MAPK/ERK, p38 MAPK and JNK. BV also activated PARP-1, MAPK/ERK. and p38 MAPK but not JNK. The expression level of anti-apoptotic molecule, Bcl-X, was decreased by VCA treatment but not by BV. Finally, the phosphorylation level of ERM proteins involved in the cytoskeleton homeostasis was decreased by both stimuli. VCA-induced apoptosis was partially inhibited by in the presence of JNK and p38 inhibitor, but BV only by p38 inhibitor. Conclusions : VCA-induced apoptosis is dependent on the activation of p38 and JNK. while BV-induced apoptosis is mediated by p38 activation in Hep G2 cells.

• Microbiology and Biotechnology Letters
• /
• v.44 no.3
• /
• pp.285-292
• /
• 2016

In the present study, we evaluated the in vitro wound-healing properties of two types of rice cell extracts (RCEs; prepared using ethanol and pressurized hot water extraction methods), using human dermal fibroblasts and keratinocytes. The effects of the RCEs (at 25–100 μg/ml) on cytotoxicity and cell migration were assessed. Both RCEs were not cytotoxic to the two cell types, instead increasing their proliferation by up to 25% in a dose-dependent manner compared with the controls. Furthermore, both RCEs significantly enhanced the migratory ability of the two cell types (fibroblast, 230–450%; keratinocyte, 170–350%). Additionally, we examined the effect of the RCEs on type I collagen synthesis, which is important in the wound reconstruction process. The RCEs significantly increased collagen type I mRNA and protein levels to a degree comparable to that induced by vitamin C. These results suggest the RCEs to be candidate materials for use in promoting wound healing, through their actions of increasing cell migration and accelerating wound re-epithelialization.

• Journal of Yeungnam Medical Science
• /
• v.9 no.1
• /
• pp.137-148
• /
• 1992

The purpose of this study was to evaluate the influence of phenobarbital(PB) on hepatotoxic effect of carbon tetrachloride($CCl_4$) which induces centrilobular necrosis in liver. Rats were injected intraperitoneally $CCl_4$ dissolved in olive oil by a dose of 0.4mg/kg. For change related to PB pretreatment, rats were injected $CCl_4$ 0.4mg/kg after PB pretreatment. The liver samples were taken in 6, 12, 24, 48, 72, and 120 hours after $CCl_4$ and/or FB injection. Extracted liver tissue was examined with light and electron microscopes. The results were sumarized as follows : 1. Light microscopic findings : In $CCl_4$ group, centrilobular necrosis developed from 6 hours after injection, was the most severe in 48 hours, and recovered after 72 hours. In addition to necrosis, fatty change and pale cell change were accompanied. In PB-$CCl_4$ group, necrosis occurred from 6 hours after $CCl_4$ injection and continued to 72 hours, and the degree of necrosis was more severe than that of $CCl_4$ group and pale cell change was decreased. 2. Electron microscopic findings: In $CCl_4$ group, the early principal change was clumping and vesicular dilatation of endoplasmic reticulum. In PB-$CCl_4$ group, the degenerative change of endoplasmic reticulum was aggrevated and the mitochondria also revealed severe degenerative change. According to the results, it was revealed that $CCl_4$ hepatotoxicity primarily began with the damage of endoplasimic reticulum, then damage of other cell organelles and cell necrosis followed, and these cytotoxic effects were aggrevated by PB pretreatment.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.3
• /
• pp.1219-1225
• /
• 2014

Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol molecule from green tea and is known to exhibit antioxidative as well as tumor suppressing activity. In order to examine EGCG tumor invasion and suppressing activity against adult T-cell leukemia (ATL), two HTLV-1 positive leukemia cells (HuT-102 and C91-PL) were treated with non-cytotoxic concentrations of EGCG for 2 and 4 days. Proliferation was significantly inhibited by 100 ${\mu}M$ at 4 days, with low cell lysis or cytotoxicity. HTLV-1 oncoprotein (Tax) expression in HuT-102 and C91-PL cells was inhibited by 25 ${\mu}M$ and 125 ${\mu}M$ respectively. The same concentrations of EGCG inhibited NF-kB nuclearization and stimulation of matrix metalloproteinase-9 (MMP-9) expression in both cell lines. These results indicate that EGCG can inhibit proliferation and reduce the invasive potential of HTLV-1-positive leukemia cells. It apparently exerted its effects by suppressing Tax expression, manifested by inhibiting the activation of NF-kB pathway and induction of MMP-9 transcription in HTLV-1 positive cells.

• Environmental Analysis Health and Toxicology
• /
• v.28
• /
• pp.7.1-7.9
• /
• 2013

Objectives We investigated the particle mass size distribution and chemical properties of air pollution particulate matter (PM) in the urban area and its capacity to induce cytotoxicity in human bronchial epithelial (BEAS-2B) cells. Methods To characterize the mass size distributions and chemical concentrations associated with urban PM, PM samples were collected by a 10-stage Micro-Orifice Uniform Deposit Impactor close to nearby traffic in an urban area from December 2007 to December 2009. PM samples for in vitro cytotoxicity testing were collected by a mini-volume air sampler with $PM_{10}$ and $PM_{2.5}$ inlets. Results The PM size distributions were bi-modal, peaking at 0.18 to 0.32 and 1.8 to $3.2{\mu}m$. The mass concentrations of the metals in fine particles (0.1 to $1.8{\mu}m$) accounted for 45.6 to 80.4% of the mass concentrations of metals in $PM_{10}$. The mass proportions of fine particles of the pollutants related to traffic emission, lead (80.4%), cadmium (69.0%), and chromium (63.8%) were higher than those of other metals. Iron was the dominant transition metal in the particles, accounting for 64.3% of the $PM_{10}$ mass in all the samples. We observed PM concentration-dependent cytotoxic effects on BEAS-2B cells. Conclusions We found that exposure to $PM_{2.5}$ and $PM_{10}$ from a nearby traffic area induced significant increases in protein expression of inflammatory cytokines (IL-6 and IL-8). The cell death rate and release of cytokines in response to the $PM_{2.5}$ treatment were higher than those with $PM_{10}$. The combined results support the hypothesis that ultrafine particles from vehicular sources can induce inflammatory responses related to environmental respiratory injury.

• The Korean Journal of Pharmacology
• /
• v.27 no.2
• /
• pp.197-205
• /
• 1991

Local extravasation during intravenous administration of adriamycin (doxorubicin HCl) can cause severe skin ulceration and necrosis. To investigate the mechanism of adriamycin-induced skin toxicity, effects of adriamycin on reactive oxygen radical metabolism using cultured skin cells of fetal rat. Adriamycin produced significant release of lactic dehydrogenase from cultured skin cell preparations dose- and time-dependently. The production of superoxide anion in sonicated suspensions of cultured skin cells was significantly increased by adriamycin under the presence of NADPH and NADH. The drug also stimulated malondialdehyde (MDA) production, an index of lipid peroxidation, in NADPH- and NADH-supported cell preparations. The increased production of MDA was significantly inhibited by oxygen radical scavengers (superoxide dismutase, catalase, thiourea) and antioxidants (butylated hydroxytoluene, ${\alpha}-tocopherol$). Treatment of cultured skin cells with 1, 3,-bis (2-chloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase, enhanced the lipid peroxidation induced by adriamycin. The present study suggests that lipid peroxidation which is resulted from the stimulated production of reactive oxygen radical causes cellular damage in adriamycin-treated skin cells of rat.

• The Korean Journal of Physiology and Pharmacology
• /
• v.17 no.4
• /
• pp.275-281
• /
• 2013

Astrocytes are reported to have critical functions in ischemic brain injury including protective effects against ischemia-induced neuronal dysfunction. Na-K ATPase maintains ionic gradients in astrocytes and is suggested as an indicator of ischemic injury in glial cells. Here, we examined the role of the Na-K ATPase in the pathologic process of ischemic injury of primary cultured astrocytes. Chemical ischemia was induced by sodium azide and glucose deprivation. Lactate dehydrogenase assays showed that the cytotoxic effect of chemical ischemia on astrocytes began to appear at 2 h of ischemia. The expression of Na-K ATPase ${\alpha}1$ subunit protein was increased at 2 h of chemical ischemia and was decreased at 6 h of ischemia, whereas the expression of ${\alpha}1$ subunit mRNA was not changed by chemical ischemia. Na-K ATPase activity was time-dependently decreased at 1, 3, and 6 h of chemical ischemia, whereas the enzyme activity was temporarily recovered to the control value at 2 h of chemical ischemia. Cytotoxicity at 2 h of chemical ischemia was significantly blocked by reoxygenation for 24 h following ischemia. Reoxygenation following chemical ischemia for 1 h significantly increased the activity of the Na-K ATPase, while reoxygenation following ischemia for 2 h slightly decreased the enzyme activity. These results suggest that the critical time for ischemia-induced cytotoxicity of astrocytes might be 2 h after the initiation of ischemic insult and that the increase in the expression and activity of the Na-K ATPase might play a protective role during ischemic injury of astrocytes.

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.40 no.4
• /
• pp.403-412
• /
• 2014

To develop an effective skin whitening agent for cosmetics, we isolated cucurbitacin B from Cucumis sativus L. which has been used as traditional skin lighting regimen by the bioactivity-guided fractionation, and investigated the inhibitory effects of cucurbitacin B on melanogenesis. At a non-cytotoxic concentration, cucurbitacin B reduced melanin contents of B16F1 melanoma cells in a dose-dependent manner. Cucurbitacin B did not directly inhibit mushroom tyrosinase activity, but it inhibited intracellular tyrosinase activity in a dose-dependent manner. Its inhibitory mechanism on melanin biosynthesis was further assessed, and we found that cucurbitacin B significantly decreased the protein level of tyrosinase, a major melanogenic enzymes and MITF, a master transcriptional factor of melanogenesis. In addition, cucurbitacin B increased the expression of WW domain-containing oxidoreductase (WWOX) which is known to function as tumor repressor and inhibits $Wnt/{\beta}$-catenin pathway. Collectively, these results suggest that cucuritacin B from C. sativus could be used as an active ingredient for skin whitening.