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Featured researches published by Si-Yun Ryu.


Molecular and Cellular Biochemistry | 2003

Quercetin suppresses proinflammatory cytokines production through MAP kinases and NF-κB pathway in lipopolysaccharide-stimulated macrophage

Sung-Yeon Cho; Sang-Joon Park; Myung-Ja Kwon; Tae-Sook Jeong; Song-Hae Bok; Woo-Young Choi; Won-Il Jeong; Si-Yun Ryu; Sun-Hee Do; Cha-Soo Lee; Jae-Chan Song; Kyu-Shik Jeong

Quercetin is a flavonoid molecule ubiquitous in nature and functions as an anti-oxidant and anti-inflammatory agent with little toxicity in vivo and in vitro. Dose- and time-dependent effect of quercetin has been investigated on proinflammatory cytokine expression and NO production, focusing on its effects on the MAP kinases and the NF-κB signal transduction pathways in LPS-stimulated RAW 264.7 cells by using RT-PCR and immunoblotting. Quercetin strongly reduced activation of phosphorylated ERK kinase and p38 MAP kinase but not JNK MAP kinase by LPS treatment. In addition, quercetin treatment inhibited NF-κB activation through stabilization of the NF-κB/IκB complex and IκB degradation and proinflammatory cytokines and NO/iNOS expression. Quercetin may exert its anti-inflammatory and immunomodulatory properties in the effect molecules such as proinflammatory cytokines and NO/iNOS by suppressing the activation of ERK and p38 MAP kinase, and NF-κB/IκB signal transduction pathways.


Materials Research Bulletin | 2003

UV and VUV characteristics of (YGd)2O3:Eu phosphor particles prepared by spray pyrolysis from polymeric precursors

E.J. Kim; Yun Chan Kang; H.D. Park; Si-Yun Ryu

Red-emitting (YGd){sub 2}O{sub 3}:Eu phosphor particles, with high luminescence efficiency under vacuum ultraviolet (VUV) and ultraviolet (UV) excitation, were prepared by a large-scale spray pyrolysis process. To control the morphology of phosphor particles under severe preparation conditions, spray solution with polymeric precursors were introduced in spray pyrolysis. The prepared (YGd){sub 2}O{sub 3}:Eu phosphor particles had spherical shape and filled morphology even after post-treatment irrespective of Gd/Y ratio. In the case of solution with polymeric precursors, long polymeric chains formed by esterification reaction in a hot tubular reactor; the droplets turned into viscous gel, which retarded the precipitation of nitrate salts and promoted the volume precipitation of droplets. The brightness of (YGd){sub 2}O{sub 3}:Eu phosphor particles increased with increasing gadolinium content, and the Gd{sub 2}O{sub 3}:Eu phosphor had the highest luminescence intensity under UV and VUV excitation. The maximum peak intensity of Gd{sub 2}O{sub 3}:Eu phosphor particles under UV and VUV were 118 and 110% of the commercial Y{sub 2}O{sub 3}:Eu phosphor particles, respectively.


Regulatory Peptides | 2001

Regulation of apoptosis by somatostatin and substance P in peritoneal macrophages.

Bit-Na Kang; Kyu-Shik Jeong; Sang-Joon Park; Sung-Ho Kim; Tae-Hwan Kim; Ho-Jun Kim; Si-Yun Ryu

Recent studies have shown that somatostatin (SOM) inhibits interleukin 6 (IL-6) and interferon gamma (IFNgamma) production by lymphocytes and peritoneal macrophages, whereas substance P (SP) enhances these cytokines production. To define the mechanism of the cytokine production enhancements and inhibitions by SOM and SP, we examined the expression of apoptosis modulator, p53, Bcl-2, Bax, inducible nitric oxide synthase (iNOS), Fas, caspase-8 and nitric oxide (NO) in thioglycolate-elicited peritoneal macrophages. SOM caused up-regulation of p53, Bcl-2, Fas and caspase-8 activities, and down-regulation of iNOS expression and NO production. On the other hand, SP slightly induces p53 and highly induces Bcl-2, iNOS expression and NO production. These data suggest that apoptosis by SOM may occur by a Bax- and NO-independent p53 accumulation, and through Fas and caspase-8 activation pathways, and that the inducible expression of Bcl-2 and NO production by SP may contribute to prevent the signals of apoptosis by Bax, and via Fas and caspase-8 activation.


Neuroimmunomodulation | 2000

Somatostatin and Substance P Induced in vivo by Lipopolysaccharide and in Peritoneal Macrophages Stimulated with Lipopolysaccharide or Interferon-Gamma Have Differential Effects on Murine Cytokine Production

Si-Yun Ryu; Kyu-Shik Jeong; Won-Kee Yoon; Sang-Joon Park; Bit-Na Kang; Sung-Ho Kim; Bae-Keun Park; Sung-Whan Cho

We have investigated whether lipopolysaccharide (LPS) induces substance P (SP) and somatostatin (SOM) in popliteal lymph nodes in vivo and whether macrophages are a source of SP and SOM in vitro. We have also investigated the effect of SP and SOM treatment on the production of cytokines. SP reached a maximum 3 days after injection of LPS (100 μg/footpad) and then declined. SOM expression after LPS injection reached a maximum at 5–7 days. Stimulation of thioglycolate-elicited peritoneal macrophages with LPS (20 μg/ml), recombinant interferon-γ (rIFN-γ, 100 U/ml), and LPS plus rIFN-γ induced SOM and SP. Thioglycolate-elicited, unstimulated peritoneal macrophages also synthesized these peptides. SOM (10–12–10–8 M) significantly inhibited IL-6 and IFN-γ production, whereas SP at those concentrations enhanced cytokine production by activated lymphocytes and macrophages. These findings suggest that neuropeptides which originate from macrophages and nerve fibers act as immunomodulators to mediate changes in the pattern of cytokine production.


Carbon | 2002

The effects of picolinic acid and pH on the adsorption of Cu(II) by activated carbon fibers

S.M Lee; Si-Yun Ryu; C.H Jung; H.J Won; W.Z Oh

Abstract The adsorption characteristics of Cu(II) on activated carbon fibers (ACFs) from simulated wastewater was investigated in the picolinic acid concentration range from 0.15 to 15 mM by varying pH from 2 to 8. When pH is below 4, the removal fraction of Cu(II) ions decreased with the decrease of pH. The removal fraction of Cu(II) ions is almost constant above pH 4. The removal efficiency of Cu(II) ions increased as the molar ratio of picolinic acid to Cu(II), specific surface area of ACFs and pH of the solution increased. In the case of [Pic]/[Cu(II)]=10, complete adsorption of Cu(II) was performed on ACF, even at pH 2.


Planta Medica | 2014

Red ginseng ameliorates acute cisplatin-induced nephropathy.

Young-Jung Kim; Mee-Young Lee; Hwa-Young Son; Bae-Keun Park; Si-Yun Ryu; Ju-Young Jung

Korean red ginseng is one of the traditional herbal medicines most widely used in China, Korea, and Japan. To determine whether Korean red ginseng extract can mitigate acute renal nephropathy, we examined its renoprotective effects in a model of cisplatin-induced acute renal failure in Sprague Dawley rats. Korean red ginseng was administered to rats by oral gavage once a day at doses of 100, 300, or 500 mg/kg for 28 days. On day 23, the animals received an intraperitoneal injection of cisplatin (5 mg/kg) to induce acute renal failure. Body weight gain, urine volume, blood urea nitrogen and creatinine concentrations, and expression of p53 were measured. Terminal deoxynucleotidyl transferase dUTP nick end-labeling was used to analyze apoptosis. Kidney tissues from the control and experimental groups were analyzed by immunohistochemistry for inflammatory cytokines and histopathological examination. To identify the mechanism responsible for the renoprotective effects of Korean red ginseng, we measured malondialdehyde concentration as an end product of lipid peroxidation and the activities of the antioxidants superoxide dismutase and glutathione. Korean red ginseng significantly decreased the levels of indicators of renal dysfunction, inflammatory cytokine expression, apoptosis, and malondialdehyde content in the kidney and also significantly attenuated the histopathological changes associated with acute renal failure. These findings suggest that Korean red ginseng has renoprotective effects against cisplatin-induced acute renal failure by reducing oxidative stress and inflammation.


Laboratory Animal Research | 2011

Chordoma in the tail of a ferret.

Eun-Sang Cho; Ju-Young Kim; Si-Yun Ryu; Ju-Young Jung; Bae-Keun Park; Hwa-Young Son

A chordoma is an uncommon tumor that originates from the remnants of the notochord and most commonly involves the cranial and caudal regions of the axial skeleton. Chordoma has been described in laboratory animals such as dogs, rats, minks, and ferrets. This report describes a case of a chordoma in the tail of a ferret. Grossly, a grayish-white, expansile, subcutaneous soft-tissue mass was observed in the tail. Histopathologically, the mass was a loosely placed, nodular, unencapsulated neoplasm within the dermis. In the mass, tumor lobules were intermingled with fibrous tissues. Fibrous tissues contained abundant extracellular basophilic material that was consistent with mucin. The tumor was composed of a close pack of adipocyte-like vacuolated cells (physaliferous cells). The cells were centrally or eccentrically located round nuclei and eosinophilic cytoplasm with large vacuoles. Immunohistologically, neoplastic cells were positive for vimentin and S-100 protein. Based on histopathologic findings and special staining characteristics, this case was diagnosed as chordoma.


Neuroimmunomodulation | 2004

Regulation of Leukocyte Function-Associated Antigen 1-Mediated Adhesion by Somatostatin and Substance P in Mouse Spleen Cells

Bit-Na Kang; Ho-Jun Kim; Kyu-Shik Jeong; Sang-Joon Park; Sung-Ho Kim; Se-Ra Kim; Tae-Hwan Kim; Si-Yun Ryu

Background: Interaction of the integrin leukocyte function-associated antigen (LFA)-1 (CD11a/CD18) with its ligands, the intercellular adhesion molecules (ICAM)-1, -2, and -3 (CD54, CD102, and CD50), is pivotal to many leukocyte adhesion events. Method: To define the mechanism of the movement of leukocytes to the inflammatory site by somatostatin (SOM) and substance P (SP), we examined the expression of the adhesion molecule LFA-1 and inside-out signals for integrins, protein kinase C (PKC), Ras, Rap1, and phosphoinositide (PI) 3-kinase, in anti-CD3-, anti-CD3+SOM-, anti-CD3+SP-stimulated or unstimulated spleen cells. Results: SOM caused down-regulation of LFA-1 mRNA translation as well as of adhesion-stimulating molecules such as Rap1, Ras, and PI 3-kinase. On the other hand, SP slightly induced LFA-1 mRNA translation and activation signals for integrins. The early-phase alteration of LFA-1 mRNA translation after 3 h of culture may be due to the changes of CD8+ T cells rather than changes of CD4+ cells. In adhesion assays, SOM significantly decreased cell adhesion (p < 0.05). Conclusion: These data suggest that SOM treatment of spleen cells, especially in CD8+ T cells, leads to downregulation of LFA-1 mRNA translation, inside-out signaling molecules for integrins (Ras, Rap1 and PI 3-kinase, but not PKC), and consequently to a decrease in the LFA-1-mediated adhesion to ICAM-1.


Biochemical and Biophysical Research Communications | 2008

Induction of apoptosis by NORE1A in a manner dependent on its nuclear export

Sang-Joon Park; Deresa Lee; Cheol-Yong Choi; Si-Yun Ryu

The RASSF family proteins were identified as tumor suppressors in a variety of human cancers, and evidenced distinct subcellular localization patterns among their subfamilies and isoforms. In this study, we showed that NORE1A was exported actively via its nuclear export signal (NES) in the C-terminus (residues 372-379). Substitutions of three lysine residues of NORE1A NES to alanines (L372, 376, 379A) showed its localization to the dot structures of the nucleus, which was similar to the NORE1A localizations observed after the administration to cells of Leptomycin B, a nuclear export inhibitor. The NORE1A NES mutant inhibited caspase-mediated apoptosis, whereas wild-type NORE1A induced caspase-3 activation. Furthermore, the NORE1A NES mutant did not co-localize with GFP-MST1, the direct downstream target of NORE1A. These results show that the nuclear export of NORE1A via NES is involved in the NORE1A-mediated induction of apoptosis.


Environmental Toxicology and Pharmacology | 2015

Expression of the Mre11–Rad50–Nbs1 complex in cisplatin nephrotoxicity

Young-Jung Kim; Tae-Won Kim; So-Ra Park; Hyun-Tae Kim; Si-Yun Ryu; Ju-Young Jung

The aim of this study was to explore whether the Mre11, Rad50, and Nbs1 (MRN) complex is associated with DNA repair mechanisms in cisplatin-induced acute renal failure. Rats were randomly allocated into three groups: control, sacrificed 5 days (5D), and 10 days (10D) after 5mg/kg of cisplatin injection. The 5D group showed disrupted renal function together with enhanced MRN complex- and DNA repair-related protein expression. Meanwhile, in the 10D group, recovery from cisplatin-induced damage was accompanied by the reduced MRN expression, although the expression was still distinctive in proximal tubular cells and higher than the control group. Moreover, pretreatment with mirin, an MRN complex inhibitor, decreased cell viability and inhibited proliferating cell nuclear antigen expression in cisplatin-treated human embryonic kidney 293 cells. Taken together, cisplatin treatment could trigger the MRN complex expression in the kidney and inhibition of the complex might aggravate damage recovery processes.

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Hwa-Young Son

Chungnam National University

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Bae-Keun Park

Chungnam National University

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Sang-Joon Park

Kyungpook National University

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Ju-Young Jung

Catholic University of Korea

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Kyu-Shik Jeong

Kyungpook National University

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Tae-Hwan Kim

Kyungpook National University

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Sung-Ho Kim

Chonnam National University

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Hyeon-Cheol Kim

Chonbuk National University

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Sung-Whan Cho

Chungnam National University

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Won-Kee Yoon

Chungnam National University

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