Sun-Hee Lee

Chonbuk National University Hospital, Sŏul, Seoul, South Korea

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Publications (4)8.7 Total impact

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    ABSTRACT: Traditional natural plants have been used throughout the world for their antidiabetic effects. The aim of the present study was to investigate the stimulating activity of a polysaccharide extract derived from T. aestivum sprout (TASP) on insulin secretion in vitro using the RIN-5F pancreatic β-cell line and rat pancreatic islets. In these experiments, TASP (0.1 to 2 mg/ml) augmented glucose-stimulated insulin secretion in a dose-dependent manner in the presence of a stimulatory glucose concentration (16.7 mM), but not of a basal concentration (1.1 mM). Although TASP failed to enhance the high K+-induced insulin secretion, the insulinotropic effect of TASP was significantly inhibited by diazoxide, an opener of ATP-sensitive K+ channel blocking insulin release. TASP potentiated the insulin secretion induced by other secretagogues, such as IBMX and tolbutamide. Moreover, glucose-derived blood insulin levels were significantly elevated by oral administration of TASP to mice, similarly to antidiabetic drugs. We also demonstrated that TASP significantly increased glucose-induced 45Ca2+ uptake and proinsulin mRNA expression in rat islets. Overall, our results suggest that TASP has a stimulating effect on insulin secretion and production in pancreatic β-cells via K+ channel closure and calcium influx. These results suggest that TASP may be useful as a candidate for the therapy of diabetes mellitus.
    International Journal of Molecular Medicine 05/2012; 29(5):913-9. · 1.96 Impact Factor
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    ABSTRACT: Serine proteases are important in the pathogenesis of intestinal inflammation. Recent studies have shown that nafamostat mesilate (NM) can inhibit the colonic mucosal inflammation induced by TNBS in rats. The aim of this study was to investigate the anti-inflammatory effects of NM on a DSS-induced colitis. Colitis was induced in female BALB/c mice by 5% dextran sulfate sodium (DSS) for 6 days. NM (2 or 20mg/kg body weight) was orally administered once a day for 6 days during treatment of the mice with DSS. The inflammatory response of the colon was assessed 1 week after DSS treatment. NM at a high dose, but not at a low dose significantly decreased disease activity index (DAI) and myeloperoxidase (MPO) induced by DSS. Furthermore, NM (20mg/kg) inhibited the production of tumor necrosis factor (TNF)-α, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the colonic tissues treated with DSS. The increase in chymase activity by DSS treatment was also attenuated by the administration of NM (20mg/kg). NM (20mg/kg) significantly decreased the colonic mucosal injury and the infiltrated mast cell number induced by DSS. These results indicate that NM might inhibit the colonic inflammation through inhibition of both chymase activity and mast cell infiltration in colon tissues of DSS-induced colitis.
    International immunopharmacology 12/2010; 11(4):412-7. · 2.21 Impact Factor
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    ABSTRACT: Oxidative stress is a pathogenesis for a typical inflammatory intestinal disease known as ulcerative colitis (UC) characterized by erosion and mucosal ulceration. For the treatment of UC, many kinds of traditional Asian medical plants have been used. Schisandra chinensis fruits (SC) are known to possess anti-ulcer, anti-hepatotoxic and anti-neurotoxic activity. However, its mechanism is still unknown. In the present study, we investigated the cytoprotective effect of deoxyschisandrin, a lignan compound comprised of SC fruits, on H2O2-induced apoptotic cell death in human intestinal epithelial cells (HCT116). In flow cytometry assay using Annexin V and propidium iodide, deoxyschisandrin inhibited H2O2-induced apoptotic cell death. To further evaluate the apoptotic signaling by H2O2, we detected caspase-3 activation using cleavage of pro-caspase-3. Deoxyschisandrin inhibited H2O2-induced caspase-3 activation by blocking cleavage of pro-caspase-3. Furthermore, it has been reported that oxidative stress by H2O2 induces an activation of nuclear factor-kappaB (NF-kappaB). In our results, H2O2 stimulated the degradation of IkappaBalpha, inhibitor of NF-kappaB, in a concentration-dependent manner. On the contrary, deoxyschisandrin inhibited H2O2-stimulated degradation of IkappaBalpha and activation of NF-kappaB by blocking translocation of NF-kappaB to the nucleus. Therefore, we suggest that deoxyschisandrin inhibits H2O2-induced apoptotic cell death.
    International Journal of Molecular Medicine 09/2010; 26(3):401-6. · 1.96 Impact Factor
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    Sun-Hee Lee, Jeong-Heon Lee, Dae-Ki Kim
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    ABSTRACT: Mast cells play a central role in the initiation and development of allergic diseases through release of various mediators. Tryptase has been known to be a key mediator in mast cell-mediated inflammatory reactions. In the present study, we investigated whether the transcription of tryptase gene in human mast cells was induced by microphthalmia (mi)-associated transcription factor (MITF). We observed that the human CD34+ progenitor-derived cultured mast cells and human mast cell line HMC-1 expressed strongly the transcripts of tryptase-beta1 and MITF-A, which is a MITF alterative splicing isoform. The transcriptional activity of tryptase gene was specifically higher in HMC-1 cells compared to the tryptase-negative cells. Using mutant constructs of tryptase promoter, we observed that two E-box (CANNTG) motifs including between -817 to -715 and -421 to -202 are able to involve in the transactivation of tryptase gene by MITF-A. In addition, the binding of these motifs-containing oligonucleotides to MITF proteins was detectable by EMGA using the nuclear extracts of HMC-1 cells and anti-MITF mAb. The overexpression of MITF-A elevated tryptase production by HMC-1 cells, while the introduction of specific siRNA against MITF attenuated the expression and enzymatic activity of tryptase. These data suggest that MITF might play a role in regulating the transcription of tryptase gene in human mast cells.
    Experimental and Molecular Medicine 05/2010; 42(5):366-75. · 2.57 Impact Factor