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- 저자 : Kang Ok-Hwa (검색결과 318 건)
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( Hwa Seon Koo ),( Hyun Jeong Yi ),( Min Young Lee ),( Min Hye Choi ),( Na Young Sung ),( Yu Im Hwang ),( In Ok Song ),( Mi Kyoung Koong ),( Inn Soo Kang ),( Kwang Moon Yang ) 대한산부인과학회 2012 대한산부인과학회 학술대회 Vol.99 No.-
Objective: To evaluate whether increased peripheral blood inflammatory immune cell can induce decrease of uterine blood flow in patients with unexplained recurrent spontaneous abortion (RSA). Methods: This study designed prospectively 33 pregnant women between 5 to 7 gestational weeks with a history of unexplained RSA included in this study. 47 normal pregnant women between 5 to 7 gestational weeks without history of infertility and/or RSA included as a control. Peripheral blood natural killer (pbNK) (CD3-/56+) fractions among peripheral blood monocyte (PBMC) were checked by flow cytometry. Uterine color-pulsed Doppler trans-vaginal ultrasound for evaluation of uterine radial artery RI was checked. Uterine radial artery resistance index (RI) compared between study and control group. After then, uterine radial artery RI was compared between high pbNK cell fraction above 12.1% among PBMC and normal pbNK cells fraction below 12.1%. Correlation between pbNK cell fraction to uterine radial artery RI was also evaluated. Results: Uterine radial artery RI in early pregnancy was significantly higher in patients with RSA than that of normal control (0.60 ± 0.14 vs. 0.54 ± 0.12, P = 0.039). Especially, the mean value of uterine radial artery RI in RSA patients with elevated pbNK cells was significantly increased than that of normal control (0.62 ± 0.13 vs. 0.54 ± 0.12, P =0.029). Otherwise, pbNK cell fractions among PBMC displayed strong positive correlation to uterine radial artery RI (Pearson`s correlation coefficient P=0.001, r = 0.667). Conclusion: Increased pbNK cells can evoke decreased uterine blood flow by their pro-inflammatory action on micro vascular structure such as uterine radial artery. This can be a one causative mechanism of inducing spontaneous abortion by increased NK cells. But, larger scaled study is needed for clarify our results.
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Tetrandrine suppresses pro-inflammatory mediators in PMA plus A23187-induced HMC-1 cells
KANG, OK-HWA,AN, HYEON-JIN,KIM, SUNG-BAE,MUN, SU-HYUN,SEO, YUN-SOO,JOUNG, DAE-KI,CHOI, JANG-GI,SHIN, DONG-WON,KWON, DONG-YEUL UNKNOWN 2014 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.33 No.5
Tetrandrine (TET), a bis-benzylisoquinoline alkaloid from the root of Stephania tetrandra, is known to possess antitumor activity in various malignant neoplasms. However, the precise mechanism of TET-mediated immune modulation remains to be clarified. One of the possible mechanisms for its protective properties is by downregulation of the inflammatory responses. In the present study, the human mast cell line (HMC-1) was used to investigate this effect. TET significantly inhibited the induction of inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 by phorbol 12-myristate 13-acetate (PMA) plus A23187. Moreover, TET attenuated expression of cyclooxygenase (COX)-2. In activated HMC-1 cells, the phosphorylation of extra-signal response kinase (ERK1/2) and c-jun N-terminal Kinase (JNK1/2), but not p38 mitogen-activated protein kinase, was decreased by treatment of the cells with TET. TET inhibited PMA plus A23187-induced nuclear factor (NF)-kappa B activation, I kappa B degradation and phosphorylation. Furthermore, TET suppressed the expression of TNF-alpha, IL-8, IL-6 and COX-2 through suppression of the ERK1/2, JNK1/2, I kappa B alpha degradation and phosphorylation, and NF-kappa B activation. These results indicated that TET exerted a regulatory effect on inflammatory reactions mediated by mast cells.
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Kang, Gi Su,Jung, Yung Hee,Kim, Hwa Su,Lee, Yeong Seon,Park, Chan,Lee, Kwang Jun,Cha, Jeong Ok The Korean Society for Laboratory Medicine 2016 Annals of Laboratory Medicine Vol.36 No.6
<P><B>Background</B></P><P>Methicillin-resistant <I>Staphylococcus aureus</I> (MRSA) are important pathogens causing nosocomial infections in Korean hospitals. This study aimed to investigate the epidemiological and genetic diversity of clinical <I>S. aureus</I> isolates in healthcare settings from 2001 to 2008.</P><P><B>Methods</B></P><P>Samples and data were obtained from 986 individuals as part of the National Antimicrobial Surveillance Project, involving 10 regions nationwide. Molecular typing studies, including multilocus sequence typing (MLST) and staphylococcal cassette chromosome <I>mec</I> (SCC<I>mec</I>) typing were performed, and a representative clone of Korean MRSA was classified by combinational grouping using a DiversiLab (DL; bioMérieux, France) repetitive element polymerase chain reaction (rep-PCR) system.</P><P><B>Results</B></P><P>Nine Korean MRSA clones (KMRSA-1 to -9) were identified by analysis of genetic backgrounds and molecular characteristics. KMRSA-1 to -3, expressing clonal complex (CC) 5 (carrying SCC<I>mec</I> II), CC8 (carrying SCC<I>mec</I> III), and CC72 (carrying SCC<I>mec</I> IV) were spread nationwide. In contrast, KMRSA-6 was highly prevalent in Gyeongsangnam-do, and KMRSA-4 was highly prevalent in Jeollanam-do and Jeollabuk-do.</P><P><B>Conclusions</B></P><P>Epidemic KMRSA clones were genetically similar to major clones identified from the USA, with the exception of KMRSA-2, which had the SCC<I>mec</I> III type. Our results provide important insights into the distribution and molecular genetics of MRSA strains in Korea and may aid in the monitoring of MRSA spread throughout the country.</P>
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Multireaction monitoring of 12 peptides for lowered immunity screening.
Kang, Min-Jung,Han, Hyojeong,Kwon, Oh-Seung,Kim, Hyun Ok,Jung, Byung-Hwa Springer-Verlag 2012 Analytical and bioanalytical chemistry Vol.404 No.8
<P>A multireaction monitoring method using high-performance liquid chromatography-tandem mass spectrometry was developed for 12 target peptides for determination of endogenous peptide concentrations in human serum. Chromatographic separation conditions were optimized and recoveries for liquid-liquid extraction, solid-phase extraction (SPE), and ultrafiltration of endogenous peptides from human serum were compared, and the SPE method was selected for 12 targeted peptide extractions. The optimized SPE method gave recoveries higher than 60 % for all targeted peptides. The limit of detection was 10 ng/ml for most peptides, except for N-formyl-methionyl-leucyl-phenylalanine (NFMLP) and adrenocorticotropic hormone (ACTH) (18-39). The limit of detection for these two peptides was 1 ng/ml. The real serum samples of 25 elderly and 23 young people were analyzed using the optimized extraction and analysis method. Half of the 12 peptides were below the limit of quantification, and B-type natriuretic peptide, cholecystokinin, ACTH(7-38), substance P, NFMLP, and valyl-glutamyl-prolyl-isoleucyl-prolyl-tyrosine were quantified in the concentration range from 0.1 to 50 ng/ml. The concentration of ACTH(7-38) was significantly higher in elderly people and that of NFMLP was significantly lower in elderly people compared with young people (p < 0.0001). This result implies that there be a possible relationships between ACTH, NFMLP and lowered immunity.</P>
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Kang, Sohi,Yang, Wonjun,Oh, Hanseul,Bae, Yeonji,Ahn, Meejung,Kang, Min Chul,Ko, Ryeo Kyeong,Kim, Gi Ok,Lee, Jun Hwa,Hyun, Jin Won,Moon, Changjong,Shin, Taekyun The Korean Society of Veterinary Science 2011 大韓獸醫學會誌 Vol.51 No.4
Several compounds and extracts isolated from a brown alga, Ishige (I.) okamurae, exhibit anti-oxidant and anti-inflammatory effects. The present study investigated whether the ethyl acetate (EtOAc) fraction of I. okamurae (EFIO) could ameliorate carbon tetrachloride ($CCl_{4}$)-induced hepatotoxicity in rats. Sprague-Dawley rats were intraperitoneally (i.p.) administered with EFIO at 10 or 50 mg/kg per day for 2 consecutive days before $CCl_{4}$ injection (3.3 mL/kg, i.p.). Twenty four hours later, the rats were anesthesized with diethyl ether and dissected. Pretreatment with EFIO significantly reduced the increased serum levels of alanine aminotransferase and aspartate aminotransferase in $CCl_{4}$-treated rats. Pretreatment with EFIO also significantly inhibited the reduced activities of superoxide dismutase and catalase in the $CCl_{4}$-injured liver. Histopathological evaluations showed that hemorrhage, hepatocyte necrosis, inflammatory cell infiltration, and fatty degeneration induced by $CCl_{4}$ treatment were ameliorated by the administration of EFIO. Additionally, liver immunohistochemical analyses revealed the marked reduction in ED1-positive monocyte-like macrophages in EFIO-pretreated rats given $CCl_{4}$. These results suggest that EFIO ameliorates $CCl_{4}$-induced liver injury, possibly through the inhibition of oxidative stress.
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Kang, Ok-Hwa,Kim, Jin-A,Choi, Yeon-A,Park, Hye-Jung,Kim, Dae-Ki,An, Yong-Hwan,Choi, Suck-Chei,Yun, Ki-Jung,Nah, Yong-Ho,Cai, Xing Fu,Kim, Young-Ho,Bae, Ki-Hwan,Lee, Young-Mi D.A. Spandidos 2005 International journal of molecular medicine Vol.15 No.6
<P>Interleukin (IL)-8 plays a central role in the initiation and maintenance of inflammatory responses in the inflammatory bowel disease. The proinflammatory cytokine-mediated production of IL-8 requires activation of various kinases, which leads to the I kappa B degradation and NF-kappa B activation. We investigated the role of 18 beta-glycyrrhetinic acid (GA), a saponin isolated from licorice roots, on TNF-alpha-induced IL-8 production in human colonic epithelial cells. HT29 cells were stimulated with TNF-alpha in the presence or absence of GA (1, 5 or 10 microM). IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction analysis, and the mitogen-activated protein kinases (MAPKs) activation and I kappa B alpha degradation were determined by Western blot analysis. GA suppressed TNF-alpha-induced IL-8 production in a concentration-dependent manner. In addition, GA inhibited TNF-alpha-induced phosphorylation of p38 MAPK and extracellular-regulated kinases (ERK), I kappa B alpha degradation, and NF-kappa B activation. These results suggest that GA has the inhibitory effects on TNF-alpha-induced IL-8 production in the intestinal epithelial cells through blockade in the phosphorylation of MAPKs, following I kappa B alpha degradation and NF-kappa B activation.</P>
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Dysfunction of Vascular Smooth Muscle and Vascular Remodeling by Simvastatin
Kang, Seojin,Woo, Hyang-Hwa,Kim, Keunyoung,Lim, Kyung-Min,Noh, Ji-Yoon,Lee, Moo-Yeol,Bae, Young Min,Bae, Ok-Nam,Chung, Jin-Ho Oxford University Press 2014 TOXICOLOGICAL SCIENCES Vol.138 No.2
<P>Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are widely prescribed for hypercholesterolemia. With the increasing use of statins, numerous reports demonstrated that statins can cause damage to skeletal muscles. However, the toxicities of statins on vascular smooth muscle, which are essential to cardiovascular homeostasis, have not been previously described. Here, we examined the effects of simvastatin on the contractile function and the integrity of vascular smooth muscle in isolated rat thoracic aortic rings, primary cultured vascular smooth muscle cells (VSMCs) <I>in vitro</I> and rats <I>in vivo</I>. In aortic rings, simvastatin suppressed the normal agonist-induced contractile responses in time- and concentration-dependent manners (0.86 g ± 0.11 at 10μM simvastatin for 24 h compared with 1.89 g ± 0.11 at control). The suppression persisted in the endothelium-denuded aortic rings and was irreversible even after wash-out of simvastatin. Simvastatin suppressed the contraction induced by Bay K8644, an activator of voltage-operated Ca<SUP>2+</SUP> channel (VOCC) in rat aortic rings and abolished agonist-induced intracellular Ca<SUP>2+</SUP> increase in VSMCs. The simvastatin-induced contractile dysfunction was reversed by the supplementation of mevalonate and geranylgeranylpyrophosphate, precursors for protein isoprenylation. Consistently, activation of RhoA, a representative isoprenylated protein, was disrupted by simvastatin in VSMCs and RhoA-mediated phosphorylation of MYPT1 and CPI-17, and tonic tension were also suppressed. Notably, prolonged treatment of simvastatin up to 48 h induced apoptosis of vascular smooth muscle in aortic rings. Most importantly, simvastatin treatment <I>in vivo</I> significantly attenuated the agonist-induced vasoconstriction in rats <I>ex vivo</I> and induced a decrease in luminal area of the vascular wall. Collectively, these results demonstrate that simvastatin can impair the normal vascular contractility by disturbing Ca<SUP>2+</SUP> influx and RhoA activity, ultimately leading to apoptosis and structural remodeling.</P>
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