Ethanol Extract of Brassica rapa ssp. pekinensis Suppresses Tumor Necrosis Factor-α-Induced Inflammatory Response in Human Umbilical Vein Endothelial Cells

주희경,최성아,이유란,이은옥,박명수,임용표,박종태,전병화 한국식품영양과학회 2017 Journal of medicinal food Vol.20 No.5

Brassica rapa L. ssp. pekinensis, commonly known as Chinese cabbage, is a cruciferous vegetable traditionally consumed in east Asia. Although its habitual consumption could account for the low incidence of chronic vascular inflammation, the therapeutic and protective potential of phytochemicals derived from Chinese cabbage has been poorly studied. In this study, we identified the phenolic compounds, kaempferol and quercetin, from the ethanol extract of Chinese cabbage (EtCC). We show for the first time that EtCC contains effective phytochemicals that suppress tumor necrosis factor (TNF)-α-induced inflammatory response in human umbilical vein endothelial cells. The EtCC inhibited TNF-a-induced monocyte adhesion to endothelial cells in a dose-dependent manner. The antiadhesive activity of EtCC directly correlated with downregulation of expression and transcription of vascular cell adhesion molecule-1 (VCAM-1). It was caused by an Nrf-2-dependent mechanism, leading to activation of antioxidant responsive element-driven promoter. Taken together, these results suggest that EtCC inhibits the expression of TNF-α-induced adhesion molecules through the indirect transcriptional modulation of VCAM-1 in endothelial cells. In conclusion, regular consumption of vegetables containing dietary phytochemicals might be a potential therapeutic strategy to protect against various stresses, to prevent several pathological conditions, and to treat chronic vascular inflammation, such as atherosclerosis.

Nanostructured polymer films from biphasic polymer latexes : application for hair cosmetics (NanoaquasomerM)

주희경,김진웅,한상훈,장이섭 한국공업화학회 2002 한국공업화학회 연구논문 초록집 Vol.2002 No.1

Protective Role of Dietary Capsanthin in a Mouse Model of Nonalcoholic Fatty Liver Disease

주희경,이유란,이은옥,김성민,Hao Jin,김수나,Yong Pyo Lim,안철근,전병화 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.6

Capsanthin is the main carotenoid compound in red paprika (Capsicum annuum L.). However, little is known about the beneficial effects of capsanthin in nonalcoholic fatty liver disease (NAFLD). In this study, the hepatoprotective activity of capsanthin was investigated in a mouse model of NAFLD. Apolipoprotein-E knockout mice were fed with normal diet, Western-type diet (WD, NAFLD model), WD with capsanthin (0.5 mg/kg of body weight/day, CAP), WD with capsanthin-rich extract (25 mg/kg of body weight/day; CRE), or WD with red paprika powder (25 mg/kg of body weight/day, RPP) for 12 weeks. The carotenoid content in CRE or RPP was analyzed using ultraperformance liquid chromatography. The capsanthin concentration in CRE was 2067 mg/100 g of dry weight, which was 63% of total carotenoids. The oral administration of CRE or capsanthin significantly reduced the WD-induced increase in body weight and lipid accumulation in the liver (vs. the RPP group). In addition, CRE or capsanthin significantly inhibited the WD-induced increase in cholesterol and low-density lipoprotein levels. Furthermore, CRE or capsanthin showed reduced levels of plasma alanine and aspartate aminotransferase (ALT and AST, respectively), suggesting a steatohepatitis protective effect. Capsanthin regulated mRNA levels of peroxisome proliferator-activated receptor alpha (Pparα), carnitine palmitoyltransferase 1A (Cpt1a), acyl-CoA oxidase 1 (Acox1), and sterol regulatory element binding protein-1c (Srebp1c), which are associated with hepatic fatty acid metabolism. Overall, our results suggest that the capsanthin of red paprika plays a protective role against hepatic steatosis/steatohepatitis in NAFLD.

pH/temperature responsive comb-type hydrogels composed of alginate and PINPAAm

주희경,김소연,이영무 한국고분자학회 1999 한국고분자학회 학술대회 연구논문 초록집 Vol.24 No.2

The 18-kDa Translocator Protein Inhibits Vascular Cell Adhesion Molecule-1 Expression via Inhibition of Mitochondrial Reactive Oxygen Species

주희경,이유란,강건,최성아,김국성,유승우,박진봉,전병화 한국분자세포생물학회 2015 Molecules and cells Vol.38 No.12

Translocator protein 18 kDa (TSPO) is a mitochondrial outer membrane protein and is abundantly expressed in a variety of organ and tissues. To date, the functional role of TSPO on vascular endothelial cell activation has yet to be fully elucidated. In the present study, the phorbol 12- myristate 13-acetate (PMA, 250 nM), an activator of protein kinase C (PKC), was used to induce vascular endothelial activation. Adenoviral TSPO overexpression (10-100 MOI) inhibited PMA-induced vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) expression in a dose dependent manner. PMAinduced VCAM-1 expressions were inhibited by Mito- TEMPO (0.1-0.5 μM), a specific mitochondrial antioxidants, and cyclosporin A (1-5 μM), a mitochondrial permeability transition pore inhibitor, implying on an important role of mitochondrial reactive oxygen species (ROS) on the endothelial activation. Moreover, adenoviral TSPO overexpression inhibited mitochondrial ROS production and manganese superoxide dismutase expression. On contrasts, gene silencing of TSPO with siRNA increased PMAinduced VCAM-1 expression and mitochondrial ROS production. Midazolam (1-50 μM), TSPO ligands, inhibited PMA-induced VCAM-1 and mitochondrial ROS production in endothelial cells. These results suggest that mitochondrial TSPO can inhibit PMA-induced endothelial inflammation via suppression of VCAM-1 and mitochondrial ROS production in endothelial cells.

Protein kinase C beta II upregulates intercellular adhesion molecule-1 via mitochondrial activation in cultured endothelial cells

주희경,이유란,최성아,박명수,강건,김국성,전병화 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.4

Activation of protein kinase C (PKC) is closely linked with endothelial dysfunction. However, the effect of PKCβII on endothelial dysfunction has not been characterized in cultured endothelial cells. Here, using adenoviral PKCβII gene transfer and pharmacological inhibitors, the role of PKCβII on endothelial dysfucntion was investigated in cultured endothelial cells. Phorbol 12-myristate 13-acetate (PMA) increased reactive oxygen species (ROS), p66shc phosphorylation, intracellular adhesion molecule-1, and monocyte adhesion, which were inhibited by PKCβi (10 nM), a selective inhibitor of PKCβII. PMA increased the phosphorylation of CREB and manganese superoxide dismutase (MnSOD), which were also inhibited by PKCβi. Gene silencing of CREB inhibited PMA-induced MnSOD expression, suggesting that CREB plays a key role in MnSOD expression. Gene silencing of PKCβII inhibited PMA-induced mitochondrial ROS, MnSOD, and ICAM-1 expression. In contrast, overexpression of PKCβII using adenoviral PKCβII increased mitochondrial ROS, MnSOD, ICAM-1, and p66shc phosphorylation in cultured endothelial cells. Finally, PKCβII-induced ICAM-1 expression was inhibited by Mito-TEMPO, a mitochondrial ROS scavenger, suggesting the involvement of mitochondrial ROS in PKC-induced vascular inflammation. Taken together, the results suggest that PKCβII plays an important role in PMA-induced endothelial dysfunction, and that the inhibition of PKCβII-dependent p66shc signaling acts as a therapeutic target for vascular inflammatory diseases.

Korean Red Ginseng Extract inhibits Tumor Necrosis Factor-alpha-induced Monocyte Adhesion in the Human Endothelial Cells

주희경,이상기,김효신,송윤정,강건,박진봉,이권호,조은정,이재환,성인환,김세훈,조충현,전병화 고려인삼학회 2008 Journal of Ginseng Research Vol.32 No.3

Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of 0.03~1 mg/ml. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.

열린 어린이집에 대한 교사의 인식에 관한 연구

주희경(Ju, Hee-Kyong),한유미(Han, You-Me) 한국영유아보육학회 2016 한국영유아보육학 Vol.0 No.97

본 연구에서는 바람직한 열린 어린이집과 열린 어린이집의 효과에 대한 교사의 인식을 알아보고 실제로 열린 어린이집 운영으로 인해 교사가 정서적 고갈을 경험하는지를 조사하고자 하였다. 이를 위해 지역과 시설유형을 안배한 어린이집 교사 340명에게 설문조사를 실시하였으며 주요 연구결과는 다음과 같다. 첫째, 열린 어린이집에 대해 잘 모르는 교사들이 많았고, 심지어 열린 어린이집 정책에 대해 반대하는 교사들도 상당수 있었다. 교사들은 완전한 개방보다는 적절한 정도의 개방을 바람직하다고 인식하고 있었다. 둘째, 교사는 열린 어린이집이 교사나 영유아보다 부모나 기관에게 긍정적 영향을 미칠 것으로 인식하고 있었다. 열린 어린이집에 대한 인식은 교사의 배경 변인에 따라 일부 차이가 있었다. 셋째, 열린 어린이집 운영과 교사의 정서적 고갈과는 관련성이 없었다. 이와 같은 연구결과들은 실효성 있는 열린 어린이집 정책을 마련하는데 중요한 시사점을 제공한다. The purpose of this study is to investigate child caregivers" awareness of the open door policy for childcare centers. It also aims to examine whether child caregivers are exhausted from the implementation of the open door policy. Three hundred and forty child caregivers participated in the survey. The main results are as follows. First, there are lots of child caregivers who don"t know about the open door policy of childcare centers, and many of them disagree with the implementation of this policy. They thought that a moderate degree of opening is desirable rather than the full opening of childcare centers. Second, they expected that the policy has a more positive effect on parents or childcare centers than on children or child caregivers. Third, child caregivers" emotional exhaustion is not related with the degree of implementation of the open door policy of the childcare centers. Implications for the successful introduction of the open door policy to childcare centers were discussed.

Ulmus davidiana ethanol extract inhibits monocyte adhesion to tumor necrosis factor-alpha-stimulated endothelial cells

이기모,주희경,이유란,박명수,강건,최성아,전병화 한국한의학연구원 2016 Integrative Medicine Research Vol.5 No.2

Background Ulmus davidiana var. japonica Rehder (UD) has long been used in traditional folk medicine in Asia. This study is designed to investigate the antiadhesive activity of the ethanol extract of UD (UDE) and its underlying mechanisms in cultured endothelial cells. Methods The dried root bark of UD was extracted with 80% (v/v) ethanol. The antiadhesive activity of the UDE was investigated in cultured human umbilical vein endothelial cells and human embryonic kidney epithelial 293T (HEK 293T) cells stably transfected with pGL3-vascular cell adhesion molecule (VCAM)-1-luc. Monocyte adhesion in endothelial cells was induced by tumor necrosis factor-alpha (TNF-α), and the protective effects of UDE on monocyte–endothelial cell adhesion, VCAM-1 expression, reactive oxygen species production, and nuclear factor-κB activity were determined. Results Exposure to UDE at a concentration of 3–30 μg/mL for 24 hours produced no detectable cytotoxicity in human umbilical vein endothelial cells, but it significantly inhibited TNF-α-induced monocyte adhesion and VCAM-1 expression. TNF-α treatment of HEK 293T/VCAM-1-luc cells resulted in increased luciferase activity of the VCAM-1 promoter, which was inhibited by treatment with UDE. Additionally, TNF-α-induced reactive oxygen species generation, nuclear translocation of nuclear factor-κB, and IκBα degradation in human umbilical vein endothelial cells were effectively reduced by treatment with 30 μg/mL of UDE. Conclusion Our results indicated that UDE treatment inhibited TNF-α-induced monocyte adhesion in endothelial cells, suggesting that UD may reduce vascular endothelial inflammation.

Dynamic Regulation of APE1/Ref-1 as a Therapeutic Target Protein

최성아,주희경,전병화 전남대학교 의과학연구소 2016 전남의대학술지 Vol.52 No.2

Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is a multifunctionalprotein that plays a central role in the cellular response to DNA damage and redoxregulation against oxidative stress. APE1/Ref-1 functions in the DNA base excision repairpathway, the redox regulation of several transcription factors, and the control ofintracellular redox status through the inhibition of reactive oxygen species (ROS)production. APE1/Ref-1 is predominantly localized in the nucleus; however, its subcellularlocalization is dynamically regulated and it may be found in the mitochondriaor elsewhere in the cytoplasm. Studies have identified a nuclear localization signal anda mitochondrial target sequence in APE1/Ref-1, as well as the involvement of the nuclearexport system, as determinants of APE1/Ref-1 subcellular distribution. Recently,it was shown that APE1/Ref-1 is secreted in response to hyperacetylation at specificlysine residues. Additionally, post-translational modifications such as phosphorylation,S-nitrosation, and ubiquitination appear to play a role in fine-tuning the activitiesand subcellular localization of APE1/Ref-1. In this review, we will introduce themultifunctional role of APE1/Ref-1 and its potential usefulness as a therapeutic targetin cancer and cardiovascular disease.