• Journal of the East Asian Society of Dietary Life
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• v.26 no.3
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• pp.207-214
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• 2016

This study investigated the effects of ginger (Zingiber officinale Roscoe) on antioxidant and antiproliferative activities in A2058 human melanoma cells. The antioxidant and antiproliferative activities of 70% ethanol extracts of Zingiber officinale Roscoe were identified based on DPPH and ABTS free radical scavenging capacities. Treatment of cells with Zingiber officinale Roscoe at concentrations of 0, 0.2, and 0.4 mg/mL for 24 hours significantly reduced cell viability as determined by Hoechst 33258 nuclear staining, apoptosis analysis, and Western blotting analysis, respectively. In our study, 70% ethanol extracts of Zingiber officinale Roscoe exhibited antioxidant activity and inhibited A2058 cell growth in a dose-dependent manner. Concomitant activation of the mitochondria-dependent apoptotic pathway of A2058 human melanoma cells by Zingiber officinale Roscoe extracts was mediated via modulation of Bax and Bcl-2 expression, which activated cleavage of caspases-3, caspases-9, and poly ADP-ribose polymerase. The findings of study indicate that Zingiber officinale Roscoe extracts induce apoptosis in A2058 human melanoma cells, and this phenomenon occurs via the death receptor-mediated and intrinsic pathways.

• Journal of Acupuncture Research
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• v.31 no.1
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• pp.121-130
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• 2014

Objectives : I investigated whether bee venom inhibit cell growth through enhancement of death receptor expressions in the human lung cancer cells, NCI-H460. Methods : Bee venom(1-5 ${\mu}g/ml$) inhibited the growth of NCI-H460 lung cancer cells by the induction of apoptotic cell death in a dose dependent manner. Results : Consistent with apoptotic cell death, expression of TNF-R1, TNF-R2, FAS, death receptors(DR) 3, 4, 5 and 6 was increased in the cells. Expression of DR downstream pro-apoptotic proteins including Caspase-8, -3, -9 was upregulated and Bax was concomitantly overwhelmed the expression of Bcl-2. NF-kB were inhibited by treatment with bee venom in NCI-H460 cells through TNF response change led by TNF-R1 and TNF-R2. Conclusions : These results suggest that bee venom should exert anti-tumor effect through induction of apoptotic cell death in NCI-H460 human lung cancer cells via enhancement of death receptor expression, and that bee venom could be a promising agent for preventing and treating lung cancer.

• Journal of Acupuncture Research
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• v.30 no.1
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• pp.57-70
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• 2013

This study was to investigated the effects of the bee venom on inhibition of cell growth via upregulation of death receptor expression in the A549 human lung cancer cells. Bee venom(1-5 ${\mu}g$/ml) inhibited the growth of A549 lung cancer cells by the induction of apoptotic cell death in a dose dependent manner. Consistent with apoptotic cell death, expression of TNFR1, Fas, death receptors(DR) 3, 4 and 6 was increased in the cells. Expression of DR downstream pro-apoptotic proteins including caspase-3, -9 and Bax was concomitantly increased, but the expression of Bcl-2, NF-${\kappa}B$ were inhibited by treatment with bee venom in A549 cells. Moreover, deletion of DR3, DR4 by small interfering RNA significantly reversed bee venom-induced cell growth inhibitory effect, whereas Apo3L strengthened anti-proliferative effect of bee venom through enhancement of DR3 expression. These results suggest that bee venom should exert anti-tumor effect through induction of apoptotic cell death in lung cancer cells via enhancement of death receptor expression, and that bee venom could be a promising agent for preventing and treating lung cancer.

• Transactions on Electrical and Electronic Materials
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• v.13 no.3
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• pp.144-148
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• 2012

In this work, we investigated to the etching characteristics of $TiO_2$ thin film and the selectivity using the inductively coupled plasma system. The etch rate and the selectivity were obtained with various gas mixing ratios. The maximum etch rate of $TiO_2$ thin film was 61.6 nm/min. The selectivity of $TiO_2$ to TiN, and $TiO_2$ to $SiO_2$ were obtained as 2.13 and 1.39, respectively. The etching process conditions are 400 W for RF power, -150 V for DC-bias voltage, 2 Pa for the process pressure, and $40^{\circ}C$ for substrate temperature. The chemical states of the etched surfaces were investigated with X-ray photoelectron spectroscopy (XPS). Its analysis showed that the etching mechanism was based on the physical and chemical pathways in the ion-assisted physical reaction.

• Korean Journal of Korean Medical Institute of Dermatology and Aesthetics
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• v.1 no.1
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• pp.16-40
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• 2005

Objective : To study the effectiveness of Yangkyuksanhawtang against Allergic Contact Dermatitis I observed the change of cutaneous shape, histochemistry, immunohistochemistry, and the distribution of apoptotic cells. materials and methods : I divided 4-month-old rats into three groups of 10, which are a contrastive group of having applied Acetone olive oil only, ACD group to have intentionally activated Allergic Contact Dermatitis by DNCB and YST group to give medication of Yangkyuksanhawtang extract. And I observed each group of mice after 24, 48 and 72 hours. results : 1. With the result of Contact hypersensitivity assay, YST group shows appreciably less ear swelling than ACD group. 2. Comparing YST and ACD groups to each other regarding general change of skin, YST group shows less hyperplasia of epidermis, less migration of inflammatory cells and less damage of epidermis than ACD group. 3. Regarding the change of collagen fiber, ACD group has appeared to be low in number of collagen fiber while YST shows similarity with the contrastive group. 4. In dermis YST group has showed lower number of mastocyte than ACD group and is granulated type. 5. In dermis YST group has showed less MAC-1, IL-1 , $IL-2R-\;{\alpha}$ G, ICAM-1 and VCAM-1 than ACD group. 6. The distribution of apoptotic cells has appeared littler in YST group than in ACD 7. Among signal molecule of apoptosis Bcl-2 has distributed more in YST group than ACD group and Bax and Fas has distributed less in YST group than ACD group.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.2
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• pp.501-507
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• 2005

Shikonin is a chemically characterized component of traditional herbal medicine, the root of Lithospermum erythrorhizon and has been shown to possess antitumor activities. Here we investigated anticancer potential of shikonin and its possible mechanism of action in LLC cells. Shikonin inhibited the proliferation of LLC cells in a concentration-dependent manner. It was also demonstrated that shikonin induced apoptosis in LLC cells by Annexin V staining and TUNEL staining analysis. Shikonin treatment was caused that decrease of Bcl-2, activation of caspases and cleavage of PARP. And shikonin also induced that the activation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38. Interestingly, the cell proliferation inhibition induced by shikonin was recovered by specific inhibitors of JNK and p38 but the inhibitor of MEK, the upstream kinase of ERK, did not recover. Additionally, shikonin administration at doses of 5 mg/kg in C57BL/6 mice strongly inhibited the primary tumor growth of LLC. Taken together, these results suggest that shikonin may suppress LLC cell proliferation by inducing an apoptotic process via activation of caspases and MAPKs

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.1
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• pp.29-35
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• 2019

Decursin is a major biological active component of Angelica gigas Nakai and is known to induce apoptosis of metastatic prostatic cancer cells. Recently, other reports have been commissioned to examine the anticancer activities of this plant. In this study, we evaluated the inhibitory activity and related mechanism of action of decursin against glioblastoma cell line. Decursin demonstrated cytotoxic effects on U87 and C6 glioma cells in a dose-dependent manner but not in primary glial cells. Additionally, decursin increased apoptotic bodies and phosphorylated JNK and p38 in U87 cells. Decursin also down-regulated Bcl-2 as well as cell cycle dependent proteins, CDK-4 and cyclin D1. Furthermore, decursin-induced apoptosis was dependent on the caspase activation in U87 cells. Taken together, our data provide the evidence that decursin induces apoptosis in glioblastoma cells, making it a potential candidate as a chemotherapeutic drug against brain tumor.

• Natural Product Sciences
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• v.24 no.3
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• pp.148-154
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• 2018

Chronic oxidative stress due to the accumulation of reactive oxygen species (ROS) in neuronal cells ultimately leads to neurodegenerative diseases. The use of natural therapies for the prevention of ROS-induced cell damage and for the treatment of neurodegenerative disorders has shown promising results. In this study, we evaluated the neuroprotective effects of the ethyl acetate (EtOAc) fraction of A. okamotoanum against the hydrogen peroxide ($H_2O_2$)-induced oxidative stress in C6 glial cells. Results show that cell viability was decreased in cells incubated with $H_2O_2$, whereas the addition of EtOAc fraction treatments in such cells significantly increased viability. The EtOAc fraction showed the highest inhibitory activity against ROS production and it also decreased the expressions of inflammatory proteins including cyclooxygenase-2, inducible nitric oxide synthase and interleukin-$1{\beta}$. Furthermore, the EtOAc fraction inhibited apoptosis by regulating the protein expressions cleaved caspase -9, -3, poly ADP ribose polymerase, Bax and Bcl-2. Therefore, these results show that the EtOAc fraction of A. Okamotoanum exhibits neuroprotective effects against $H_2O_2$ induced oxidative damage by regulating the inflammatory reaction and apoptotic pathway.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2943-2948
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• 2012

Arsenic exposure is a serious health hazard worldwide. We have previously established that it may result in immune suppression by upregulating Th2 cytokines while downregulating Th1 cytokines and causing lymphocytic death. Treatment modalities for arsenic poisoning have mainly been restricted to the use of chelating agents in the past. Only recently have combination therapies using a chelating agent in conjunction with other compounds such as anti-oxidants, micronutrients and various plant products, been introduced. In the present study, we used T11TS, a novel immune potentiating glycopeptide alone and in combination with the sulfhydryl-containing chelator, mono-iso-amyl-dimarcaptosuccinic acid (MiADMSA) as a therapeutic regimen to combat arsenic toxicity in a mouse model. Results indicated that Th1 cytokines such as TNF-${\alpha}$, $IFN{\gamma}$, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen. Similar results were obtained with the apoptotic proteins studied, FasL, BAX, BCL2 and the caspases 3, 8 and 9, where again T11TS proved more potent than in combination with MiADMSA in preventing lymphocyte death. The results thus indicate that T11TS alone is more efficient in immune re-establishment after arsenic exposureas compared to combination therapy with T11TS+MiADMSA.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.12
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• pp.5071-5076
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• 2014

Cholangiocarcinoma (CCA) is one of the aggressive cancers with a very poor prognosis. Several efforts have been made to identify and develop new agents for prevention and treatment of this deadly disease. In the present study, we examined the anticancer effect of luteolin on human CCA, KKU-M156 cells. Sulforhodamine B assays showed that luteolin had potent cytotoxicity on CCA cells with IC50 values of $10.5{\pm}5.0$ and $8.7{\pm}3.5{\mu}M$ at 24 and 48 h, respectively. Treatment with luteolin also caused a concentration-dependent decline in colony forming ability. Consistent with growth inhibitory effects, luteolin arrested cell cycle progression at the G2/M phase in a dose-dependent manner as assessed by flow cytometry analysis. Protein expression of cyclin A and Cdc25A was down-regulated after luteolin treatment, supporting the arrest of cells at the G2/M boundary. Besides evident G2/M arrest, luteolin induced apoptosis of KKU-M156 cells, demonstrated by a distinct sub-G1 apoptotic peak and fluorescent dye staining. A decrease in the level of anti-apoptotic Bcl-2 protein was implicated in luteolin-induced apoptosis. We further investigated the effect of luteolin on JAK/STAT3, which is an important pathway involved in the development of CCA. The results showed that interleukin-6 (IL-6)-induced JAK/STAT3 activation in KKU-M156 cells was suppressed by treatment with luteolin. Treatment with a specific JAK inhibitor, AG490, and luteolin diminished IL-6-stimulated CCA cell migration as assessed by wound healing assay. These data revealed anticancer activity of luteolin against CCA so the agent might have potential for CCA prevention and therapy.