http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Involvement of heme oxygenase-1 in Korean colon cancer.
Kang, Kyoung Ah,Maeng, Young Hee,Zhang, Rui,Yang, Young Ro,Piao, Mei Jing,Kim, Ki Cheon,Kim, Gi Young,Kim, Young Ree,Koh, Young Sang,Kang, Hee Kyoung,Hyun, Chang Lim,Chang, Weon Young,Hyun, Jin Won Saikon Pub. Co 2012 TUMOR BIOLOGY Vol.33 No.4
<P>Heme oxygenase-1 (HO-1) catabolizes heme into carbon monoxide, biliverdin, and free iron which mediate its protective effect against oxidative stress. The aim of the present study was to determine the expression level and activity of HO-1 in Korean colon cancer tissues and cell lines. HO-1 protein expression was higher (>1.5-fold) in tumor tissues than in adjacent normal tissues in 14 of 20 colon cancer patients, and HO-1 protein expression was closely correlated with HO-1 enzyme activity in cancer tissues. Immunohistochemical data confirmed that HO-1 protein was expressed at a higher level in colon cancer tissues than in normal mucosa. Furthermore, HO-1 mRNA and protein expression and enzyme activity were higher in the colon cancer cell lines Caco-2, SNU-407, SNU-1033, HT-29, and SW-403 than in the normal fetal human colon cell line FHC. Treatment with the HO-1 inhibitor zinc protoporphyrin decreased the viability of colon cancer cell lines. These data indicate that HO-1 may serve as a clinically useful biomarker of colon cancer and as a target for anticolon cancer drugs.</P>
Kang, Kyoung Ah,Wang, Zhi Hong,Zhang, Rui,Piao, Mei Jing,Kim, Ki Cheon,Kang, Sam Sik,Kim, Young Woo,Lee, Jongsung,Park, Deokhoon,Hyun, Jin Won Molecular Diversity Preservation International (MD 2010 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.11 No.11
<P>Recently, we demonstrated that myricetin exhibits cytoprotective effects against H<SUB>2</SUB>O<SUB>2</SUB>-induced cell damage via its antioxidant properties. In the present study, myricetin was found to inhibit H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic bodies, nuclear fragmentation, sub-G<SUB>1</SUB> cell population, and disruption of mitochondrial membrane potential (Δψ<I><SUB>m</SUB></I>), which are increased in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Western blot data showed that in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells, myricetin increased the level of Bcl-2, which is an anti-apoptotic factor, and decreased the levels of Bax, active caspase-9 and -3, which are pro-apoptotic factors. And myricetin inhibited release of cytochrome c from mitochondria to cytosol in H<SUB>2</SUB>O<SUB>2</SUB>-treated cells. Myricetin-induced survival correlated with Akt activity, and the rescue of cells by myricetin treatment against H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis was inhibited by the specific PI3K (phosphoinositol-3-kinase) inhibitor. Myricetin-mediated survival also inhibited the activation of p38 mitogen activated protein kinase (MAPK) and c-Jun <I>N</I>-terminal kinase (JNK), which are members of MAPK. Our studies suggest that myricetin prevents oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.</P>
Anticancer Effects of 23-Dihydroganoderic Acid N
Kang Kyoung-Ah,Zhang Rui,Piao Mei Jing,Kim Ju-Sun,Kang Sam-Sik,Hyun Jin-Won Korean Environmental Mutagen Society 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.4
23-Dihydroganoderic acid N, a triterpenoid compound, was investigated whether it may show cytotoxic activity against U937, HeLa, NCI-H460 and MCF-7 cancer cells by MTT test. As a result, 23-dihydroganoderic acid N show sensitive to MCF-7 cells among NCI-H460, HeLa, U937, and MCF-7 cells.
Preventive Effect of 7,8-Dihydroxyflavone against Oxidative Stress Induced Genotoxicity
Zhang, Rui,Kang, Kyoung Ah,Piao, Mei Jing,Ko, Dong Ok,Wang, Zhi Hong,Chang, Weon Young,You, Ho Jin,Lee, In Kyung,Kim, Bum Joon,Kang, Sam Sik,Hyun, Jin Won Pharmaceutical Society of Japan 2009 Biological & pharmaceutical bulletin Vol.32 No.2
<P>We elucidated the protective effect of 7,8-dihydroxyflavone against hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>)-induced DNA damage. We found that 7,8-dihydroxyflavone scavenges 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and intracellular reactive oxygen species (ROS). 7,8-Dihydroxyflavone with antioxidant effect prevented the H<SUB>2</SUB>O<SUB>2</SUB>-induced cellular DNA damage, as evidenced by comet tail, 8-hydroxy-2′-deoxyguanosine (8-OHdG) content, and phospho-histone H2A.X protein expression. Hence, 7,8-dihydroxyflavone was shown to protect cell <I>via</I> the inhibition of apoptosis induced by H<SUB>2</SUB>O<SUB>2</SUB>. This was substantiated by decreased apoptotic nuclear fragmentation, decreased sub-G<SUB>1</SUB> cell population, and decreased DNA fragmentation. Furthermore, 7,8-dihydroxyflavone activated the protein kinase B (PKB, Akt) signal pathway, which is a major survival signal pathway. In addition, LY294002, which is phosphatidylinositol 3 kinase (PI3K, upstream of Akt) inhibitor, attenuated the protective effect of 7,8-dihydroxyflavone against H<SUB>2</SUB>O<SUB>2</SUB>-induced cell damage. In conclusion, 7,8-dihydroxyflavone was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing Akt activity.</P>
Morin (2′,3,4′,5,7‐Pentahydroxyflavone) Protected Cells against γ‐Radiation‐Induced Oxidative Stress
Zhang, Rui,Kang, Kyoung Ah,Kang, Sam Sik,Park, Jae Woo,Hyun, Jin Won Blackwell Publishing Ltd 2011 Basic & Clinical Pharmacology & Toxicology Vol.108 No.1
<P><B>Abstract: </B> Ionizing radiation can induce cell damage by generating reactive oxygen species (ROS). The present study was carried out to investigate the radio‐protective effects of a flavonoid compound, morin (2′,3,4′,5,7‐pentahydroxyflavone) and the underlying mechanisms. Morin was found to reduce the intracellular ROS generated by γ‐irradiation. Moreover, morin protected cellular components against radiation‐induced membrane lipid peroxidation and cellular DNA damage, which are the main targets of radiation‐induced cell damage. Morin recovered cell viability damaged by radiation via inhibition of apoptosis. Irradiated cells with morin treatment reduced Bax, phospho Bcl‐2, active caspase 9 and caspase 3, which were induced by γ‐radiation. Irradiated cells with morin recovered the expression of Bcl‐2 reduced by γ‐radiation. Morin exerted anti‐apoptotic effects via inhibition of mitogen‐activated protein kinase kinase‐4 (MKK4/SEK1)‐c‐Jun NH<SUB>2</SUB>‐terminal kinase (JNK)‐activator protein 1 (AP‐1) cascades induced by γ‐radiation. The results suggest that morin protects cells against oxidative stress induced by radiation via reduction of ROS and attenuation of SEK1‐JNK‐AP‐1 pathway.</P>
산화적 스트레스에 대한 복합 한약재의 항 산화활성 검색
강경아(Kyoung Ah Kang),장예(Rui Zhang),강대길(Dae Gill Kang),김진숙(Jin Sook Kim),현진원(Jin Won Hyun) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.1
Reactive oxygen species (ROS) are known to cause oxidative modification of DNA, proteins, lipids and small cellular molecules and are associated with tissue damage and are the contributing factors for diabetes, inflammation, aging, cancer, arteriosclerosis, and hypertension. We screened the anti-oxidative effect on V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with eleven extracts of combined medicinal plants. Dancheonhwankakambang and Samikangyabtang were found to show the scavenging activities of DPPH radical and intracellular reactive oxygen species, which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA).
Kang, Kyoung Ah,Zhang, Rui,Piao, Mei Jing,Lee, Kyoung Hwa,Kim, Bum Joon,Kim, So Young,Kim, Hee Sun,Kim, Dong Hyun,You, Ho Jin,Hyun, Jin Won Informa Healthcare 2007 Free radical research Vol.41 No.6
<P> The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H2O2 treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H2O2 induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.</P>
Kang, Kyoung-Ah,Zhang, Rui,Piao, Mei-Jing,Park, Min-Jeong,Kwon, Ae-Ran,Kim, Bum-Joon,You, Ho-Jin,Chung, Myung-Hee,Hyun, Jin-Won Korean Society for Biotechnology and Bioengineerin 2007 Biotechnology and Bioprocess Engineering Vol.12 No.2
8-Hydroxydeoxyguanosine $(oh^8dG)$ treatment induced senescence-like changes in KG-1 cells, a human acute myelocytic leukemia cell line. The $oh^8dG-treated$ cells stained positive for senescence associated ${\beta}-galactosidase$ $(SA-{\beta}-galactosidase)$ and had enlarged cell shape, both of which are senescence indexes. The $oh^8dG-treated$ cells were also cell growth inhibited and arrested at $G_1$ in the cell cycle. The accumulation of cdk (cyclin dependent kinase) inhibitors, such as p16, p21, and p27, also implies that cellular senescence was induced in $oh^8dG-treated$ cells. However, these changes were not accompanied by cell differentiation or telomerase activity. Taken together, we conclude that $oh^8dG$ treatment of KG-1 cells induces cellular senescence.