• The Journal of Korean Medicine
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• v.31 no.2
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• pp.137-148
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• 2010

Objective: This study aimed to evaluate the protective effects of Gamipalmi-hwan (GPH) on elastase-induced lung cell injury. Materials and Methods: As an in vitro model of emphysema, the current study was performed to investigate potential activity of GPH in regulating injury responses of A549 human type II cell line mediated by elastase treatment. Results: GPH treatment increased the number of A549 cells which was reduced by elastase digestion. Elastin protein level, which was reduced by elastase treatment, was increased by GPH treatment. Labeling intensity with caspase 3 protein in elastase-treated cells was reduced by GPH treatment. Both Erk1/2 and Cdc2 protein levels, which were decreased by elastase treatment, were increased to a level similar to that of the normal cells. mRNA levels encoding IL-$1{\beta}$ and TNF-$\alpha$ were increased by elastase and then down-regulated by GPH. Conclusion: The present data suggest that A549 cells are subjected to inflammatory damage by elastase and can be recovered by GPH treatment. Further studies examining the protective activity of GPH in elastase-treated lung tissue would be useful for therapeutic strategies of emphysema treatment.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.983-987
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• 2014

Nigella sativa (N sativa), commonly known as black seed, has been used in traditional medicine to treat many diseases. The antioxidant, anti-inflammatory, and antibacterial activities of N sativa extracts are well known. Therefore, the present study was designed to investigate the anticancer activity of seed extract (NSE) and seed oil (NSO) of N sativa against a human lung cancer cell line. Cells were exposed to 0.01 to 1 mg/ml of NSE and NSO for 24 h, then percent cell viability was assessed by 3-(4, 5-dimethylthiazol-2yl)-2, 5-biphenyl tetrazolium bromide (MTT) and neutral red uptake (NRU) assays, and cellular morphology by phase contrast inverted microscopy. The results showed NSE and NSO significantly reduce the cell viability and alter the cellular morphology of A-549 cells in a concentration dependent manner. The percent cell viability was recorded as 75%, 50%, and 26% at 0.25, 0.5, and 1 mg/ml of NSE by MTT assay and 73%, 48%, and 23% at 0.25, 0.5, and 1 mg/ml of NSE by NRU assay. Exposure to NSO concentrations of 0.1 mg/ml and above for 24 h was also found to be cytotoxic. The decrease in cell viability at 0.1, 0.25, 0.5, and 1 mg/ml of NSO was recorded to be 89%, 52%, 41%, and 13% by MTT assay and 85%, 52%, 38%, and 11% by NRU assay, respectively. A-549 cells exposed to 0.25, 0.5 and 1 mg/ml of NSE and NSO lost their typical morphology and appeared smaller in size. The data revealed that the treatment of seed extract (NSE) and seed oil (NSO) of Nigella sativa significantly reduce viability of human lung cancer cells.

• Journal of Acupuncture Research
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• v.20 no.5
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• pp.93-106
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• 2003

Objective : To investigate the possible molecular mechanism(s) of melittin as a candidate of anti-cancer drug, we examined the effects of the compound on the growth of human lung carcinoma cell line A549. Methods: MTT, morphological changes, DAPI staining, Western blot, RT-PCR and in vitro prostaglandin E2 (PGE2) accumulation assays were performed. Results: The anti-proliferative effect by melittin treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. Melittin induced apoptotic cell death in a concentration-dependent manner, which was associated with inhibition or degradation of apoptotic target proteins such as ${\beta}$-catenin, poly(ADP-ribose) polymerase(PARP) and phospholipase $C-{\gamma}1(PLC-{\gamma}1)$. Melittin treatment inhibited the expression of cyclooxygenase-2(COX-2) and accumulation of PGE2 in aconcentration-dependent fashion. In addition, Melittin treatment induced the down-regulation of telomerase reverse transcriptase(hTERT) and proto-oncogene c-myc expression of A549 cells. Conclusions: Taken together, these findings suggest that melittin-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and melittin may have therapeutic potential in human lung cancer.

• Korean Journal of Environmental Agriculture
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• v.29 no.4
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• pp.421-426
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• 2010

Benzene is one of volatile environmental pollutants to induce asthma and allergy in respiratory system. The airway epithelium is a physical barrier to inhaled toxicants and particulates. However, the effect of benzene in lung epithelial cell viability has not been elucidated. Thus, this study was conducted to investigate the effect of benzene on apoptosis in A549 cells, lung epithelial cell line. In this study, benzene decreased cell viability of A549 cells in a dose-dependent manner (> $10{\mu}M$). Benzene-induced decrease of cell viability was blocked by the treatment of antioxidants (vitamin C and NAC). Indeed, benzene induced lipid peroxide formation in A549 cells. Benzene decreased Bcl-2 expression but increased Bax expression in A549 cells. In addition, benzene also increased the cleaved form of caspase-3. In conclusion, benzene induced apoptosis via oxidative stress in cultured epithelial cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.2
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• pp.553-560
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• 2004

In the present study, we investigated the anti-proliferative effects of aqueous extract of Wikyung-tang(WKT) on the growth of human lung carcinoma cell line A549. WKT treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effects by WKT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. WKT treatment induced an inhibition and/or degradation of apoptotic target proteins such poly(ADP-ribose) polymerase (PARP) and phospholipase C-γ1 (PLC-γ1). WKT treatment did not affect the levels of other Bcl-2 family gene products, such as Bcl-2, Bax and Bad. Western blot analysis and RT-PCT data revealed that the levels of tumor suppressor p53 and cyclin-dependent kinase inhibitor p21 were induced by WKT treatment in A549 cells. Additionally, WKT treatment induced the down-regulation of telomerase reverse transcriptase mRNA (hTERT) expression of A549 cells, however, the levels of other telomere-regulatory gene products were not affected. Taken together, these findings suggest that WKT-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products and WKT may have therapeutic potential in human lung cancer.

• Food Science and Preservation
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• v.24 no.2
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• pp.289-293
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• 2017

Ethanol extract of garlic peels (GPE) was investigated for its antiproliferative effects on human cancer cell lines. Human lung cancer cell line A549 treated with $500{\mu}g/mL$ GPE resulted in the growth inhibition of A549 by 90%. In stomach cancer cell AGS proliferation inhibition activity, GPE showed 45% and 71% inhibition of AGS growth at $1,000{\mu}g/mL$ and $2,000{\mu}g/mL$, respectively. GPE inhibited the growth of the breast cancer cells MCF-7 effectively at low concentration and showed 78% and 90% inhibitions of MCF-7 growth at $200{\mu}g/mL$ and $500{\mu}g/mL$, respectively. GPE showed very significant antiproliferation effect on liver cancer cell line Hep3B and inhibited Hep3B cell growth by 57% at $100{\mu}g/mL$, and the inhibition's rate increased up to 87% at $500{\mu}g/mL$. Antiproliferation effect of GPE on colorectal cancer cell HT-29 showed 15% reduction of HT-29 cell growth at $200{\mu}g/mL$ and the growth rate was reduced in a dose dependent manner up to $1,000{\mu}g/mL$. These results indicated that GPE had high antiproliferation effects on breast and liver cancer cell lines at low concentrations ($200{\mu}g/mL$), and by higher concentrations over $500{\mu}g/mL$, GPE inhibited the growth of A549 and HT-29. The results of our study suggested the potential use of garlic peels for use as an excellent antiproliferative substance for human cancer cells.

• Journal of Digital Policy
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• v.2 no.1
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• pp.31-35
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• 2023

This study was conducted to examine the effect of Broccoli Extract on the proliferation inhibition of human-derived cancer cells and the degree of inhibition. The three cell lines used in the experiment were respiratory system lung cancer cells A549, digestive system liver cancer cells SNU-182 and biliary tract cancer SNU-1196. All cancer cells were derived from the human body, and the CCK-8 method was used to measure the degree of inhibition of cancer cell proliferation. As a result of examining the effect on Broccoli Extract 10ug/mL, 100ug/mL, 1000ug/mL, Broccoli Extract inhibited proliferation in a concentration-dependent manner in most cancer cells, In particular, lung cancer cell A549 and liver cancer cell SNU-182 showed significant proliferation inhibition at 1000ug/mL.As a result, it can be seen that broccoli extract provides potential as a cancer preventive and therapeutic agent for tumor suppression mechanisms proven through cell experiments.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.6115-6120
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• 2013

Introduction: Some non-small cell lung cancer (NSCLC) tumor cells are insensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) -based therapy. This study was conducted to examine the effect of embelin on the sensitivity of the A549 NSCLC cell line to TRAIL receptor2 (TRAILR2) monoclonal antibodies and to investigate the potential mechanisms. Materials and Methods: A549 cells were treated with embelin, TRAILR2 mAb or a combination of both. Cell viability was measured using ATPlite assay and apoptosis rates were determined by flow cytometry with AnnexinV-FITC and propidium iodide staining, with the expression levels of proteins analyzed by Western blotting. Results: The cell survival rate of separate treatments with 100 ng/ml TRAILR2 antibody or 25 uM embelin were $81.5{\pm}1.57%$ and $61.7{\pm}2.84%$, respectively. Their combined use markedly decreased cell viability in A549 cells to $28.1{\pm}1.97%$ (P<0.05). The general caspase inhibitor Z-VAD-FMK could inhibit the embelin-enhanced sensitivity of A549 cells to TRAILR2 mAb ($75.97{\pm}3.17%$)(P<0.05). Both flow cytometry and cell morphological analysis showed that embelin was able to increase TRAIL-induced apoptosis in A549 cells. Combined treatment with embelin and TRAILR2 mAb augmented the activation of initiator caspases and effector caspase. In addition, A549 cells showed increasing levels of TRAILR2 protein and decreasing levels of Bcl-2, survivin and c-FLIP following the treatment with embelin+TRAILR2 mAb. Conclusions: Embelin could enhance TRAIL-induced apoptosis in A549 cells. The synergistic effect of the combination treatment might be due to modulation of multiple components in the TRAIL receptor-mediated apoptotic signaling pathway, including TRAILR2, XIAP, survivin, Bcl-2 and c-FLIP.

• Journal of Chest Surgery
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• v.38 no.4 s.249
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• pp.263-270
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• 2005

In recent years, a combination of two demographic phenomena, an increased number of older people in the population and an increase in the incidence of lung cancer with age, has made it mandatory to develop therapeutic modalities with less toxicity for the treatment of inoperable elderly patients with lung cancer. Therefore, we investigated the correlation between COX-2 expression and cytotoxicity of Nimesulide, a specific COX-2 inhibitor. Material and Method: Immunohistochemical staining of COX-2 was performed. After exposure of Nimesulide, XTT analysis, FACS analysis and Hoechst staining were carried out. Result: COX-2 protein was expressed in non-treated A549 cells strongly, but not in H1299. Cytotoxicity of Nimesulide against A549 cell and H1299 cell were similar and $IC_{50}$ of Nimesulide in both cell lines were $70.9{\mu}M$ in A549 cell line and $56.5{\mu}M$ in H1299 cell line respectively. FACS analysis showed $G_0/G_1$ arrest in both cell lines and the S phase cell fraction was decreased. Morphologic assessment of apoptosis by Hoechst 33258 staining, many apoptotic cells were detected in both cell lines. Conclusion: Selective COX-2 inhibitor, Nimesulide, can inhibit the proliferation of non-small cell lung cancer cell lines in vitro. Inhibitory effect of Nimesulide are induction of apoptosis and $G_0/G_1$ arrest. There is no correlation between COX-2 expression and cytotoxicity of Nimesulide, a specific COX-2 inhibitor. Therefore, highly selective COX-2 inhibitors such as Nimesulide can be expected to lead to even greater efficacy of their use as adjuncts to various anticancer angents and radiation therapy for the treatment of high-risk patients.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.5
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• pp.682-689
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• 2014

This study was carried out to discriminate the effects of the ramie leaf according to the drying methods (hot air drying and freeze drying) on antioxidative activity in vitro and antiproliferation in human cancer cells. There were no significant differences in total polyphenol content of ramie leaf ethanol extracts depending on the drying methods, but total flavonoid content was significantly higher in hot air dried ramie leaf (HR) than in freeze dried ramie leaf (FR). The DPPH radical scavenging activity of HR and FR ethanol extracts were found to be 77.74%, and 77.29% in 1000 ppm, respectively. Antioxidative index of HR and FR ethanol extracts measured by Rancimat were lower than those in BHT, BHA, and ascorbic acid, but were higher than that in control. The antiproliferation effect of 80% ethanol extracts of HR and FR on liver cancer cell line (H460), stomach cancer cell line (AGS), and lung cancer cell line (A549) were increased with a dose-dependent manner. The cancer cell growth inhibition activities of HR and FR ethanol extracts at the concentration of $800{\mu}g/mL$ showed greater than 80% on Hep G2 and A549 cell line, and greater than 75% on AGS cell line. These results suggest that HR and FR ethanol extracts possess potential antioxidative effect and antiproliferation in human cancer cells, and those activities of ramie leaf ethanol extracts depending on the drying methods were similar.