Poster 발표 논문 초록 - 생화학 / 분자생물학 / 생리학 분야 PP-09 : 귀리 Avenacosidase ( β-glucosidase ) Isozyme 의 유전자 Cloning 및 대장균에서 Multimer 형태로 발현

강구성,김용우,김인수 한국응용생명화학회(구 한국농화학회) 1999 한국응용생명화학회 학술발표회 Vol.1999 No.1

혈우병 환자에서의 공장경색증

강구성,김유사,강중신 大韓消化器病學會 1985 大韓消化器病學會誌 Vol.17 No.2

Genistein과 Daidzein이 대장암 HCT-116 세포의 성장에 미치는 영향

신종헌,강구성,김정옥,윤길숙,권태균,김정완,손윤경 대한병리학회 2006 Journal of Pathology and Translational Medicine Vol.40 No.1

Background : Genistein and daidzein are two major soybean isoflavones. They have received increasing attention because of their possible roles for cancer prevention. However, their mechanisms of action and molecular targets on the human colon cancer cells are not fully understood. Methods : Human colon cancer HCT-116 cells were treated with genistein and daidzein to investigate their effects on the cell growth and this was analyzed with MTT assay. TUNEL assay and Hoechst33342 stain were carried out to identify apotosis. Results : Daidzein was able to inhibit cell proliferation and induce apoptosis of the HCT-116 cells, but genistein didn't affect the cell growth. The ER antagonist ICI182780 didn’t attenuate the antiproliferative and proapoptotic effects of daidzein: this means the effect of daidzein on the HCT-116 cells may not be dependent on the ER pathway. The other soybean isoflavone, genistein, attenuated the effects of daidzein on the HCT-116 cells and its mechanism should be elucidated. Conclusions : These data suggest that daidzein may act as a preventive agent on human colon cancer, and its mechanism of action doesn’t involve the ER-dependent pathway.

쥐 해마의 Lipopolysaccharide 국소주입에 의한 Tumor Necrosis Factor-α, Interleukin-1β 및 Inducible Nitric Oxide Synthase의 발현

오훈규,강구성,김지연,곽은경,김정완,박지영,손윤경 대한병리학회 2004 Journal of Pathology and Translational Medicine Vol.38 No.3

Background : Brain inducible nitric oxide synthase (iNOS) might be detectable in several pathologic conditions, and it is thought to play an important role in their pathophysiology. Tumor necrosis factor (TNF)- and interleukin (IL)-1 are believed to be essential factors of iNOS induction of the brain. Methods : After intrahippocampal stereotaxic injection of lipopolysaccharide (LPS), the rat brains were removed at 6, 12 and 24 h. The rat brain tissues were examined to clarify the expression patterns of TNF- , IL-1 and iNOS. Results : The inflammatory cells which were stained with anti-TNF- antibody, appeared in 6 h and increased for 24 h after LPS injection. The iNOS positive cells appeared after 12 h of LPS injection. A semiquantitative analysis of reverse transcription-polymerase chain reaction (RT-PCR) revealed that the TNF- and IL-1 mRNA arose at 1 h, peaked at 6 h and then declined until 48 h after LPS injection. The iNOS mRNA arose after 6 h, peaked at 12 h, and declined until 48 h after LPS injection. Conclusions : We conclude that the induction of inflammatory events by intrahippocampal injection of LPS activates TNF- and IL-1 secretion, and this is followed by an induction of iNOS expression. TNF- and IL-1 seem to be related with iNOS expression in brain inflammation.

세계의 포장 - 이지필 실런트

유야정인,강구성 한국포장협회 2015 包裝界 Vol. No.

Lipopolysaccharide/Interferon-gamma에 의한C6 Glioma 세포주의 Nitric Oxide 생성 양상과Dexamethasone의 억제효과

신종헌,강구성,김지연,김선주,박지영,곽은경,손윤경 대한병리학회 2002 Journal of Pathology and Translational Medicine Vol.36 No.6

Background : Glial cell-derived nitric oxide (NO), and its regulation has significant implications for central nervous system pathophysiology. The aim of the present study was to see the production of NO in lipopolysaccharide (LPS)/interferon-gamma (IFN-α)-treated C6 glioma cells and the effect of dexamethasone on NO production and apoptosis of LPS/IFN-α-treated C6 glioma cells. Methods : The apoptosis of LPS/IFN-α treated C6 glioma cell was examined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method and the production of NO in culture medium was measured. The expression of iNOS mRNA was examined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The effect of the N-monomethyl L-arginine (NMMA) and dexamethasone on the apoptosis and NO production was also examined. Results : Inducible nitric oxide synthase (iNOS) mRNA and NO production were markedly increased in LPS/IFN-α- treated C6 glioma cells. The expression of iNOS mRNA arose at 3 hours, peaked at 12 hours, and declined 24 hours after LPS/IFN-α-treatment. Accumulation of NO derivatives in the culture media was increased at least upto 48 hours after LPS/IFN-α. The induction of iNOS expression and NO production in LPS/IFN-α-treated C6 cells was correlated with apoptotic cell death judged by TUNEL staining. After treatment of NMMA, one of the NOS inhibitors, NO production and apoptosis were markedly decreased. Dexamehasone treatment suppressed the NO production by concentration depenedent manner. Conclusions : From the above results it is concluded that the LPS/IFN-α induced apoptosis of C6 cells is mediated by iNOS-derived NO and NO production and apoptosis was suppressed by dexamethasone.

Ginsenoside Rb1이 C6 Glioma 세포주의 Nitric Oxide 생성과 세포자멸사에 미치는 효과

박주현,이윤희,강구성,이수경,김선주,박지영,곽은경,손윤경 대한병리학회 2004 Journal of Pathology and Translational Medicine Vol.38 No.1

Background : Ginsenosides, the extract of Panax ginseng, exert various pharmacological effects such as anticancer activity by the mechanism that is not yet defined. In this study, we proposed that the anticancer effect of ginsenoside Rb1 is related to tumor cell apoptosis and ginsenoside Rb1 induces the tumor cell apoptosis via the nitric oxide (NO) production. Methods : Rat C6 glioma cells were activated by treating with lipopolysaccharide (LPS), interferon (IFN)- , and tumor necrosis factor (TNF)- on the culture medium to investigate the effects of ginsenoside Rb1. Results : Compared with C6 glioma cells treated with LPS/IFN- /TNF- , C6 glioma cells treated with LPS/IFN- /TNF- /ginsenoside Rb1 showed marked increase in the NO production and apoptosis. Ginsenoside Rb1 induces the NO production in C6 glioma cells in dose-dependent manner. When C6 glioma cells treated with LPS/IFN- /TNF- /ginsenoside Rb1 were incubated with the specific inhibitor of iNOS, S-Methyl-2-thiopseudoureasulfate (SMT), both NO production and apoptosis in C6 glioma cells was significantly decreased. Ginsenoside Rb1 induced the expression of iNOS mRNA and iNOS protein in C6 glioma cells. Conclusions : These results suggest that the induction of iNOS expression and subsequent

유방암 세포주(T47D와 MDA-MB231)에서 Genistein의 세포주기 G2/M 정지 기전

손윤경,박지영,강구성 한국유방암학회 2010 Journal of breast cancer Vol.13 No.4

Purpose: To analyze the effect of the growth control on human breast cancer cells with genistein treatment and to investigate the mechanism of genistein-induced G2/M arrest in T47D and MDA-MB231 breast carcinoma cells by Cdc25C expression. Methods: We analysed the proliferartion of the two cell lines by using MTT proliferation assay, flow cytometric analysis, real-time quantitative RT-PCR and western blotting and investigated the effect of genistein on cell survival, cellular toxicity, cell cycle progression-related genes and their mRNA and protein alterations. Results: The DNA flow cytometric analysis of both cell lines treated with genistein showed a dose-dependent growth inhibition and accumulation in the G2/M phase of cell cycle. The expression of p21 mRNA and protein increased in both cell lines following genistein treatment but p27 expression was unchanged. Furthermore,decreased Cdc25C expression with decreased polo-like kinase (PLK) 1 expression and increased PLK3 expression were observed after genistein treatment. The decreased level of Cdc25C in the nucleus was associated with decreased phosphorylation of Cdc25C by PLK1. The expression of PLK3was increased with a dose-dependent and a time-dependent manner and was associated with decreased Cdc25C expression. Check point kinase (CHK) 1 and CHK2 revealed different expression patterns each other. The CHK1 expression was independent of the presence of genestein. CHK2 expression increased in MDA-MB231 cells associated with decreased Cdc25C expression but not in T47D. Conclusion: These results suggest that genistein induces a G2/M arrest in human breast cancer cells, the mechanism of which is due, in part, to decreased in Cdc25C phosphatase by a regulatory effect of PLK1, PLK3, and CHK2 as well as increased expression of the cyclin dependent kinase inhibitor p21(WAF1/CIP1).

PC12 세포주에서 Lipopolysaccharide/Tumor Necrosis Factor-α/Interferon-γ로 유도된 Inducible Nitric Oxide Synthase 발현과 세포자멸사

김지연,김지영,강구성,곽은경,박지영,박태인,손윤경 대한병리학회 2002 Journal of Pathology and Translational Medicine Vol.36 No.4

Inducible nitric oxide synthase (iNOS) has been detected in a number of pathologic conditions in the central nervous system. This study was investigated the patterns of iNOS expression in the neuronal PC12 cell and the effects of nitric oxide on the apoptosis of PC12 cells. Methods : The stimulating agents for induction of iNOS expression in PC12 cells were bacterial lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-α), and interferon- gamma (IFN-γ). Results : The expression iNOS mRNA and protein in PC12 cells stimulated with LPS/TNF-α/IFN-γ were profoundly increased. The expression of iNOS mRNA arose at 6 hours, peaked at 12 hours, and declined to 48 hours after LPS/TNF-α/IFN-γ treatment. iNOS protein was increased up to 24 hours in LPS/TNF-α/IFN-γ treated PC12 cells while the expression of nNOS was unaffected. Accumulation of NO derivatives in the culture media was markedly increased at least at up to 48 hours after LPS/TNF-α/IFNtreatment. The induction of iNOS expression and NO production in differentiated PC12 cells was correlated with apoptotic cell death judged by transmission electron microscopy and DNA fragmentation from the results of the Terminal deoxynucleotidyl-transferase-mediated dUDP biotin nick end-labeling (TUNEL) method. After treatment with NOS inhibitor, Nmonomethylarginine (NMMA), a profound decrease in NO production by LPS/TNF-α/IFN-γ treated PC12 cells was noted. And the LPS/TNF-α/IFN-γ induced apoptosis was prevented by the NMMA treatment. Conclusions : From the above results it is concluded that the expression of iNOS in differentiated PC12 cells is induced by the combined application of LPS, TNF-α, and IFN-γ . And the apoptosis of cultured PC12 cells is mediated by iNOSderived NO.

일시적 국소 뇌허혈손상에서 신경세포의 세포자멸사와 Inducible Nitric Oxide Synthase 발현

이병육,황성규,강구성,전홍화,이영미,김정완,곽은경,박지영,손윤경 대한병리학회 2004 Journal of Pathology and Translational Medicine Vol.38 No.6

Background : Neuronal death in acute-phase cerebral ischemic injury is caused by necrosis. However, neuronal injury after reperfusion can be associated with apoptosis. Methods : We used Sprague-Dawley rats whose brains were reperfused after middle cerebral artery occlusion for either 30 min or 2 h. We examined a relationship between apoptosis and the expression of inducible nitric oxide synthase (iNOS) in the brain tissue from 3 h to 14 days after reperfusion in both groups. Results : TUNEL and iNOS positivity were closely related in both groups. The 2-h ischemia group exhibited increases in the amount of TUNEL and iNOS-positive cells for up to 3 days after reperfusion, at which the TUNEL and iNOS-positive cells decreased. The 30-min ischemia group exhibited peak positivity 24 h after reperfusion, followed by a similar decrease. iNOS mRNA expression peaked 3 h after reperfusion in the 30-min ischemia group, at which time it decreased. In the 2-h ischemia group, iNOS mRNA increased 3 h after reperfusion, peaked 24 h after reperfusion, and then decreased. Conclusions : These results indicated the occurrence of delayed apoptosis in transient cerebral ischemia. Increased expression of iNOS is closely associated with this apoptosis, and oxygen free radical-producing materials, such as nitric oxide, may play an important role in the induction of this apoptosis.