• Korean Journal of Environmental Agriculture
• /
• v.23 no.4
• /
• pp.228-233
• /
• 2004

Nitrate removal was examined from May to October 2003 of a surface flow treatment wetland cell, which was a part of a treatment wetland system composed of four wetland cells and a distribution pond The system was established on rice paddy near the Kohung Estuarine Lake located in the southern part of the Korean Peninsula. Effluent from a secondary-level night soil treatment plant was funneled into the system. The investigated cell, 87 m in length and 14 m in width, was created in April 2003. An open water was designed at its center, which was equivalent to 10 percent of its total area. Cattails (Typha angustifolia) were transplanted from natural wetlands into the cell and their stems were cut at about 40cm height from their bottom ends. Average $25.0\;m^3/day$ of effluent from the treatment plant was funneled into the cell by gravity flow and average $24.1\;m^3/day$ of its treated effluent was discharged into the Sinyang Stream flowing into the lake. Its water depth was maintained about 0.2 m and its hydraulic detention time averaged 5.2 days. Average height of the cattail stems was 42.5 cm in May 2M3 and 117.7 cm in September 2003. The number of stems averaged $9.5\;stems/m^2$ in May 2003 and $16.4\;stems/m^2$ in September 2003. The growth of cattails was good. Temperature of influent and effluent averaged 25.9 and $26.7^{\circ}C$, respectively. $NO_3$-N loading rate of influent and effluent averaged 176.67 and $88.09\;mg/m^2\;day$, respectively. Removal of rf03-N averaged $89.58\;mg/m^2\;day$ and its removal rate by mass was about 50%. Considering its initial operating stage in which cattail rhizomes and litter layer on the bottom were not Idly established, the $NO_3$-N removal rate of the cell was rather good.

• Tuberculosis and Respiratory Diseases
• /
• v.75 no.6
• /
• pp.231-235
• /
• 2013

Knowledge of molecular pathogenesis of non-small cell lung cancer has increased remarkably and changed the principles of treatment, especially during the past decade. These advancements have been limited mainly to adenocarcinoma of the lung. Recently, genetic alterations in squamous cell lung cancer (SQCLC) have been detailed and positive results of clinical trials using agents targeting these changes have indicated the potential for improved treatment outcomes for SQCLC.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.22 no.4
• /
• pp.821-828
• /
• 2008

Onchungeum, a herbal formula, which has been used for treatment of anemia due to bleeding, discharging blood and skin disease. In the present study, it was examined the effects of extract of Onchungeum (OCE) on the growth of human hepatocarcinoma cell lines Hep3B (p53 null type) and HepG2 (p53 wild type) in order to investigate the anti-proliferative mechanism by OCE. Treatment of Hep3B and HepG2 cells to OCE resulted in the growth inhibition in a dose-dependent manner, however Hep3B cell line exhibited a relatively strong anti-proliferative activity to OEC. Flow cytometric analysis revealed that OCE treatment in Hep3B cells caused G1 phase arrest of the cell cycle, which was associated with various morphological changes in a dose-dependent fashion. RT-PCR and immunoblotting data revealed that treatment of OCE caused the down-regulation of cyclin D1 expression, however the levels of cyclin E expression were not changed by OCE. The G1 arrest of the cell cycle was also associated with the induction of Cdk inhibitor p27 by OCE. Because the p53 gene is null in Hep3B cells, it is most likely that the induction of p21 is mediated through a p53-independent pathway. Moreover, p27 detected in anti-Cdk4 and anti-Cdk2 immunoprecipitates from the OCE-treated cells, suggesting that OCE-induced p27 protein blocks Cdk kinase activities by directing binding to the cyclin/Cdk complexes. Furthermore, OCE treatment potently suppresses the phosphorylation of retinoblastoma proteins and the levels of the transcription factor E2F-1 expression. Taken together, these results indicated that the growth inhibitory effect of OCE in Hep3B hepatoma cells was associated with the induction of G1 arrest of the cell cycle through regulation of several major growth regulatory gene products.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.27 no.6
• /
• pp.511-518
• /
• 2001

The effect of mycolactone, a recently reported apoptosis-inducing factor, was investigated in SCC15 oral squamous cell carcinoma(OSCC) cell line. Mycolactone rapidly induced cell death in OSCC cells in 2days, which was similar to that found in apoptotic cell such as detaching from culture plate and rounding-up of cells. Apoptotic cells were increased 4hrs after mycolactone treatment and more than half of cells showed apoptosis after 72hrs. Caspase 3 activation a biochemical evidence of apoptosis, was determined by Western blotting. Caspase 3 activation was started at 2hrs that lasted until 8hrs after mycolactone treatment. The expression of bcl-2 family genes was determined to explain the mechanism of apoptosis found in OSCC cells. The expressions of bad, bak, and bax (pro-apoptotic genes) and bcl-w and bcl-2 genes (anti-apoptotic genes) were not changed by mycolactone treatment. The expression of bcl-xi was decreased 8 hrs after mycolactone treatment. Mcl-1 expression was initially increased at 2 hrs which was decreased 8 hrs after mycolactone treatment. The down-regulation of these two anti-apoptotic genes might explain the mycolactone-induced apoptosis in OSCC cells. In this study, mycholactone was revealed to induce cell death in OSCC cells apoptosis and the apoptosis mechanism of OSCC cells was shown to be down-regulation of anti-apoptotic genes, bcl-xi and mcl-1. These results suggested the applicability of mycolactone for the development of an anti-cancer drug candidate by inducing apoptosis of OSCC cancer cell.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.16 no.6
• /
• pp.1177-1183
• /
• 2002

We investigated the effects of Sabaek-san (SBS) water extract on the cell proliferation of human lung carcinoma A549 cells. SBS treatment resulted in the inhibition of cell proliferation in a concentration-dependent manner. This anti-proliferative effect of A549 cells by SBS treatment was associated with morphological changes such as membrane shrinking and cell rounding up. DNA flow cytometric histograms showed that population of G1 phase of the cell cycle was increased by SBS treatment in a concentration-dependent manner. SBS treatment induced a marked accumulation of tumor suppressor p53 and a concomitant induction of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP, which appears to be transcriptionally upregulated and is p53 dependent. In addition, SBS treatment resulted in down-regulation of cyclooxygenase-2 (COX-2) as determined by RT-PCR analysis. The present results indicated that SBS-induced inhibition of lung cancer cell proliferation is associated with the blockage of G1/S progression the induction of apoptosis.

• Biomolecules & Therapeutics
• /
• v.26 no.3
• /
• pp.328-334
• /
• 2018

Because of the unsatisfactory treatment options for breast cancer (BC), there is a need to develop novel therapeutic approaches for this malignancy. One such strategy is chemotherapy using non-toxic dietary substances and botanical products. Studies have shown that Panduratin A (PA) possesses many health benefits, including anti-inflammatory, anti-bacterial, anti-oxidant and anticancer activities. In the present study, we provide evidence that PA treatment of MCF-7 BC cells resulted in a time- and dose-dependent inhibition of cell growth with an $IC_{50}$ of $15{\mu}M$ and no to little effect on normal human MCF-10A breast cells. To define the mechanism of these anti-proliferative effects of PA, we determined its effect critical molecular events known to regulate the cell cycle and apoptotic machinery. Immunofluorescence and flow cytometric analysis of Annexin V-FITC staining provided evidence for the induction of apoptosis. PA treatment of BC cells resulted in increased activity/expression of mitochondrial cytochrome C, caspases 7, 8 and 9 with a significant increase in the Bax:Bcl-2 ratio, suggesting the involvement of a mitochondrial-dependent apoptotic pathway. Furthermore, cell cycle analysis using flow cytometry showed that PA treatment of cells resulted in G0/G1 arrest in a dose-dependent manner. Immunoblot analysis data revealed that, in MCF-7 cell lines, PA treatment resulted in the dose-dependent (i) induction of $p21^{WAF1/Cip1}$ and p27Kip1, (ii) downregulation of Cyclin dependent kinase (CDK) 4 and (iii) decrease in cyclin D1. These findings suggest that PA may be an effective therapeutic agent against BC.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.19 no.4
• /
• pp.1062-1067
• /
• 2005

The purpose of this study was to examine the inhibition effect of Zizania latifolia that has been used heart disease, Diabetes Mellitus and Skin disease for a long time on apoptosis induced by $H_2O_2$ in Neuro2A cell. Neuro2A cells were cultivated in RPMI(GibcoBRL) with $5\%$, FBS and treated with $H_2O_2$, and Zizania latifolia. We measured the cell viability and analyzed DNA fragmentation. Activity of PARP, Cytochrome C, caspase-9, caspase-3, p53, p21, Bax and Bcl-2 in the cell was examined by using western blot. The cell viability in Zizania latifolia treatment (60ug/ml<) decreased significantly compared with that of none treatment. (p<0.001) Zizania latifolia increased cell viability about twice as much as that being injury by $H_2O_2$. (Zizania Latifolia 20ug/ml, $H_2O_2$ 200uM, P<0.001) DNA fragmentation developed by $H_2O_2$, but was not developed in Zizania latifolia treatment. PARP, Cytochrome C, caspase-9 and caspase-3 activated all by $H_2O_2$ but were not activated in Zizania latifolia treatment.. P53, P2l and Bu activated by $H_2O_2$, and Bcl-2 got into inactivation. But the opposite results appeared in Zizania latifolia treatment. In conclusion, these results suggest that Zizania latifolia inhibit the development of DNA fragmentation and apoptosis by $H_2O_2$ and the antioxidant action of Zizania latifolia is effective. More researches about effect of Zizania latifolia are considered to need.

• The Korean Journal of Physiology and Pharmacology
• /
• v.5 no.1
• /
• pp.79-86
• /
• 2001

Recent clinical studies have shown that a high proportion of patients with acute promyelocytic leukemia (APL) achieve complete remission after treatment with all-trans retinoic acid (ATRA). However, most patients who receive continuous treatment with ATRA relapse and develop ATRA-resistant leukemia. Dendritic cells (DCs) are important antigen-presenting cells in the development of antileukemic T-cell responses. In this study, we investigated the strategies to overcome ATRA resistance of APL cells by inducing the differentiation of DCs from human leukemic cell lines for the developtment of adoptive immunotherapy. CD83 was used as a mature DC marker in this study and the expression of CD83 mRNA was determined by RT-PCR method. The promyelocytic leukemic cell line HL-60, B lymphoblast cell lines RPMI 7666 and NC-37 could be induced to dendritic cells in vitro. Treatment of HL-60 with phorbol 12-myristate 13-acetate (PMA) resulted in the expression of myeloid-related DC phenotypes, while treatment of RPMI 7666 with fms-like tyrosine kinase 3 ligand (Flt3-ligand, FL) and treatment of NC-37 with PMA and FL led to the expression of lymphoid-related DC phenotypes. In conclusion, myeloid-related DC phenotypes and lymphoid-related DC phenotypes could be generated from HL-60, NC-37 and RPMI 7666 cell lines, respectively. These DC phenotypes can potentially be used to generate antileukemic T cells in vitro for adoptive immunotherapy.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.20 no.1
• /
• pp.149-155
• /
• 2006

To prevent human body injury from oxidative stress, antioxidants are very important and many research about antioxidants are generally being conducted. Hydrogen peroxide($H_2O_2$) that is one of vitality oxygen species has been seen that cause various diseases, DNA damage and gene change. The purpose of this study was to examine the inhibition effect of Zizania latifolia Rhizoma on apoptosis induced by $H_2O_2$ in Neuro2A cell. Neuro2A cells were cultivated in RPMI(GibcoBRL) with 5% FBS and treated with $H_2O_2$ and Zizania latifolia Rhizoma. We measured the cell viability and analyzed DNA fragmentation. Activity of PARP, Cytochrome C, caspase-9, caspase-3, p53, p21, Bax and Bcl-2 in the cell was examined dy using western blot. The results obtained were as Follows: The cell viability in Zizania latifolia Rhizoma treatment (60ug/ml<) decreased significantly compared with that of none treatment. (P<0.001) Zizania latifolia Rhizoma increased cell viability about twice as much as that being injury by $H_2O_2$. (Zizania Latifolia Rhizoma 20ug/ml, $H_2O_2$ 200uM, P<0.001) DNA fragmentation developed by $H_2O_2$, but was not developed in Zizania latifolia Rhizoma treatment. PARP, Cytochrome C, caspase-9 and caspase-3 activated all by $H_2O_2$ but were not activated in Zizania latifolia Rhizoma treatment. P53, P2l and Bax activated dy $H_2O_2$, and Bcl-2 got into inactivation. But the opposite results appeared in Zizania latifolia Rhizoma treatment. In conclusion, these results suggest that Zizania latifolia Rhizoma inhibit the development of DNA fragmentation and apoptosis by $H_2O_2$ and the antioxidant action of Zizania latifolia Rhizoma is effective. More researches about effect of Zizania latifolia Rhizoma are considered to need.

• Journal of Acupuncture Research
• /
• v.19 no.3
• /
• pp.41-50
• /
• 2002

Objective : To study anti-inflammatory, analgesic effect and molecular biological mechanism of honey bee venom for aqua-acupuncture, human mast cell line(HMC-1) and human glioma cell line(HS683) were treated with bee venom. Methods : Cell viability of bee venom was tested by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) asssay. To explore whether anti-inflammatory, analgesic effects of bee venom are associated with the control of gene expression, quantitative RT-PCR analysis of inflammation and pain related genes was performed. Results : The MTT assay demonstrated that cell viability was not decreased by treatment with 10-9 ug/ml bee venom in comparison with 10-2, 10-3, 10-4, 10-5, 10-6, 10-7, 10-8, 10-9, 10-10 and 10-11 ug/ml. sPLA2 and COX-l were down-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line in comparison with control. COX-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HS683 Cell line and HSP-2 was up-regulated by treatment with 10-9 ug/ml bee venom in HMC-1 Cell line in comparison with control. sPLA2, COX-1 and COX-2 showed no significant regulation in HMC-1 Cell line and cPLA2 also showed no significant regulation in both HMC-l and HS683 Cell line between control and bee venom treated group.