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한주은,강경아 대한류마티스 건강전문학회 2000 근관절건강학회지 Vol.7 No.1
The arthritis patients suffer from psychological, social and spiritual problems as well as physical problems because the arthritis is not curable and has chronic pain, joint deformity, limitation of activity and physical dysfunction for all of his life. Especially if they do not fond the meaning in their lives, they will experience spiritual distress seriously. Therefore, it is important that nurses help the patients to find the meaning in their lives and to reduce spiritual distress. The purpose of this study is to provide a basis for nursing intervention strategies to minimize the arthritis patients' spiritual distress and understand the relationship between the meaning of life and the spiritual distress in arthritis patients. The samples were composed of 157 arthritis patients. Data collection was carried out from October 1, 1998 to February 28, 1999. Data were analyzed using a SAS Program for descriptive statistic, Pearson correlation, t-test, ANOVA, linear regression. The results were as follow, 1. The scores on the meaning of life scale ranged from 51 to 130 with a mean of 93. 2. The scores on the spiritual distress scale ranged from 26 to 91 with a mean of 60. 3. There were significant correlations between the meaning of life and the spiritual distress(r=.53, p=.00). 4. The linear regression analysis showed that the meaning of life explained 13% of the spiritual distress. 5. In the degree of the meaning of life and the spiritual distress according to the general characteristics, the level of the meaning of life in arthritis patients was different by the duration of incidence(F=2.71, p=.03). In conclusion, the nursing intervention strategies to reduce the spiritual distress in arthritis patients must take into account the meaning of life.
박영만,임영,강성규,김지홍,이종욱,최용휴,김경아 大韓産業醫學會 1999 대한직업환경의학회지 Vol.11 No.2
Aplastic anemia is characterized by pancytopenia with hypocellular bone marrow. Fifty percent of the cases are idiopathic and the rest are caused by various agents including drugs, chemicals, radiation and viruses. It is difficult to link specific etiologic agents, especially chemicals to the development of aplastic anemia because multiple or unknown exposures may be involved in. Benzene, a common industrial chemical and a component of gasoline, may lead progressively to pancytopenia, aplastic anemia and leukemia when exposed. A petrochemical worker with aplastic anemia was referred to our hospital to evaluate a relationship between the job history and the disease. He worked in the petrochemical plant for 21 years and was exposed to low-level benzene. There was not anyother etiologic agent except benzene and this is the case report of aplastic anemia which possibly due to benzene exposure.
Cytoprotective Effects of KIOM-79 on Streptozotocin Induced Cell Damage by Inhibiting ERK and AP-1
Kang, Kyoung Ah,Lee, Kyoung Hwa,Kim, So Young,Kim, Hee Sun,Kim, Jin Sook,Hyun, Jin Won Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.5
<P>The present study investigated the potential cytoprotective properties of a combination of plant extracts (KIOM-79) obtained from <I>Magnolia officinalis</I>, <I>Pueraria lobata</I>, <I>Glycyrrhiza uralensis</I>, and <I>Euphorbia pekinensis</I>, against the oxidative stresses induced by streptozotocin (STZ) in a rat pancreatic β-cells (RINm5F). KIOM-79 was found to scavenge intracellular reactive oxygen species (ROS), thereby preventing DNA damage and lipid peroxidation. The KIOM-79 inhibited apoptosis of the β-cells exposed to STZ <I>via</I> radical scavenging activity and activation of antioxidant enzymes. KIOM-79 inhibited activation of extracellular regulated kinase (ERK) induced by STZ and inhibited DNA binding activity of an activator protein-1 (AP-1), a downstream transcription factor of ERK. Taken together, these findings suggest that KIOM-79 protects against STZ induced cell death in RINm5F cells by inhibiting ROS generation and the ERK pathway.</P>
Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
Kang, Kyoung Ah,Piao, Mei Jing,Ryu, Yea Seong,Hyun, Yu Jae,Park, Jeong Eon,Shilnikova, Kristina,Zhen, Ao Xuan,Kang, Hee Kyoung,Koh, Young Sang,Jeong, Yong Joo,Hyun, Jin Won Spandidos Publications 2017 International journal of oncology Vol.51 No.4
<P>The present study determined whether luteolin induces HT-29 colon cancer cell death through an antioxidant effect such as the activation of antioxidant enzymes. Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC). Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells. Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol, and increased the levels of the active forms of caspase-9 and caspase-3. Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells. Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis. The apoptotic effect of luteolin was mediated by the activation of the mitogen-activated protein kinase signaling pathway. The present results indicate that luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.</P>
Kang, Kyoung Ah,Piao, Mei Jing,Hyun, Yu Jae,Zhen, Ao Xuan,Cho, Suk Ju,Ahn, Mee Jung,Yi, Joo Mi,Hyun, Jin Won Nature Publishing Group UK 2019 Experimental and molecular medicine Vol.51 No.4
<▼1><P>Luteolin, a dietary flavone, modulates various signaling pathways involved in carcinogenesis. In this study, we investigated the molecular mechanism that underlies the apoptotic effects of luteolin mediated by DNA demethylation of the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter and the interaction of Nrf2 and p53, a tumor suppressor, in human colon cancer cells. Luteolin increased the expression of apoptosis-related proteins and antioxidant enzymes. In DNA methylation, luteolin inhibited the expression of DNA methyltransferases, a transcription repressor, and increased the expression and activity of ten-eleven translocation (TET) DNA demethylases, a transcription activator. Methyl-specific polymerase chain reaction and bisulfite genomic sequencing indicated that luteolin decreased the methylation of the Nrf2 promoter region, which corresponded to the increased mRNA expression of Nrf2. In addition, luteolin increased TET1 binding to the Nrf2 promoter, as determined using a chromatin immunoprecipitation (ChIP) assay. TET1 knockdown decreased the percentages of luteolin-treated cells in sub-G<SUB>1</SUB> phase and cells with fragmented nuclei. Furthermore, complex formation between p53 and Nrf2 was involved in the apoptotic effects of luteolin. These results provide insight into the mechanism that underlies the anticancer effects of luteolin on colon cancer, which involve the upregulation of Nrf2 and its interaction with the tumor suppressor.</P></▼1><▼2><P><B>Cancer: Cell-killing plant compound exerts antioxidant effects</B></P><P>A molecule found in fruits, vegetables and herbs helps kill colon cancer cells by activating a master regulator of detoxifying enzymes. Jin Won Hyun from Jeju National University School of Medicine in South Korea and colleagues treated human colon cancer cells with luteolin, a molecule that occurs naturally in many food plants. They showed that luteolin increased the levels of proteins involved in cell death and antioxidant responses by causing DNA-modifying enzymes to strip suppressive chemical markers off the gene encoding Nrf2, a protein that regulates antioxidant effects. Nrf2 levels subsequently increased and the protein interacted with the tumor suppressor p53 to facilitate destruction of the colon cancer cells. The findings offer a mechanistic basis for using luteolin to help prevent and treat cancer.</P></▼2>
Induction of Antioxidant Enzymes in Phloroglucinol Treated Cells
Kyoung Ah Kang,Kyoung Hwa Lee,Sungwook Chae,Rui Zhang,Myung Sun Jung,Young Min Ham,Jong Seok Baik,Nam Ho Lee,Jin Won Hyun 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.4
We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown seaweed), against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Phloroglucinol was found to scavenge intracellular reactive oxygen species (ROS) generated by γ-ray radiation. In addition, phloroglucinol inhibited cell damage induced by radiation through scavenging ROS. Phloroglucinol increased the superoxide dismutase and glutathione peroxidase activity. Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant enzymes activity.
Kyoung Ah Kang,김진숙,Rui Zhang,Mei Jing Piao,Weon Young Chang,김기천,Gi Young Kim,진미림,Jin Won Hyun 한국생물공학회 2009 Biotechnology and Bioprocess Engineering Vol.14 No.3
KIOM-4 is a plant extract obtained from Magnolia offcinalis, Pueraria lobata, Glycyrrhiza uralensis, and Euphorbia pekinen-sis. Previously, we reported that KIOM-4 protects pancreatic β-cells against streptozotocin (STZ) induced oxidative stress. To elucidate the cytoprotective mechanism of KIOM-4 on oxidative stress, we focused on the induction of heme oxygenase- 1 (HO-1), which plays a role in cytoprotection against oxidative injury as well as providing an important function in the maintenance of homeostasis, in rat pancreatic β-cells (RINm5F). In this study, we showed that KIOM-4 up-regulated HO-1 expression at the mRNA and protein levels, thus resulting in increased HO-1 activity. HO-1 induction is regulated at the transcriptional level and is mediated by a specific enhancer, the antioxidant response element (ARE), which is found in the promoter of HO-1 gene. The transcription factor, NF-E2 related factor 2 (Nrf2), interacts with the ARE to activate HO-1 gene transcription and results in the modulation of HO-1 expression. KIOM-4 increased the nuclear translocation, ARE binding, and transcriptional activity of Nrf2. In addition, the extracellular regulated kinase (ERK) positively contributed to ARE-driven HO-1 expression. Furthermore, KIOM-4 elicited the activation of ERK and U0126 (inhibitor of ERK) attenuated the KIOM-4 induced activation of Nrf2, which subsequently decreased HO-1 protein levels. These findings suggest that the induction of HO-1 by KIOM-4 is dependent on the ERK pathway. Taken together, KIOM-4 enhances the cellular antioxidant defense system through the induction of HO-1 via the ERK-Nrf2-ARE signaling pathway, thereby protecting cells from streptozotocininduced cell damage
Kang, Kyoung-Ah,Chae, Sung-Wook,Lee, Kyoung-Hwa,Zhang, Rui,Jung, Myung-Sun,You, Ho-Jin,Kim, Jin-Sook,Hyun, Jin-Won The Korean Society for Biotechnology and Bioengine 2005 Biotechnology and Bioprocess Engineering Vol.10 No.6
Homogentisic acid was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals and thus prevented lipid peroxidation in human fibroblast (Wl 38) cells. The radical scavenging activity of homogentisic acid was found to protect Wl 38 cells against hydrogen peroxide $(H_2O_2)$ induced oxidative stress, via the activation of extracellular signal regulated kinase (ERK) protein. Homogentisic acid increased the activity of catalase. Hence, from the present study, it is suggested that homogentisic acid protects Wl 38 cells against $H_2O_2$ damage by enhancing the intracellular antioxidative activity.