Sun-Hee Lee

Chonbuk National University, Tsiuentcheou, Jeollabuk-do, South Korea

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Publications (6)10.09 Total impact

  • Sun-Hee Lee · Sung-Won Lim · Young-Mi Lee · Hoi-Seon Lee · Dae-Ki Kim ·
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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. DOI:10.3892/ijmm.2012.905 · 2.09 Impact Factor
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    ABSTRACT: Type 2 diabetes mellitus (NIDDM) is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. In order to control the type 2 diabetes mellitus, anti-hyperglycemic effect of Triticum aestivum L. water extracts (TAWE) was investigated in 7 week old male diabetic C57BL6/J-ob/ob mice. For the experiments, the diabetic animal model ob/ob mice and non-diabetic animal model lean mice were divided into 3 groups: non-treatment control group (Control), and two experimental groups orally treated with 25 or 100 mg/kg/day dose of TAWE (TAWE-25 and TAWE-100, respectively). The lean mice were used as the non-diabetic normal control. TAWE was orally administrated for 6 weeks and the diabetic clinical markers, including blood glucose level, body weight, organs weight and insulin level were determined. The oral administration of TAWE-100 in ob/ob diabetic mice significantly decreased blood glucose level (78.4%) and body weight (11.9%) compared with diabetic control group. The weights of organs, including spleen, liver, kidneys, heart and lung were not different among groups, while the treatments of TAWE-100 in ob/ob diabetic mice significantly reduced blood total cholesterol (24.35%) and triglyceride (23.97%) levels compared with the diabetic control group. The levels of serum insulin and glucose tolerance were improved after TAWE-100 treatment in ob/ob diabetic mice. Moreover, the immunohistochemical staining for insulin detection in pancreatic islet -cells expressed high level of insulin in TAWE-100 treated ob/ob mice. From the above results, the intake of TAWE may be effective in anti-hyperglycemia by the attenuation of glucose and lipid levels. TAWE-containing diets or drugs may be beneficial for controlling diabetes mellitus type 2 in human.
    Journal of the Korean Society of Food Science and Nutrition 03/2011; 40(3). DOI:10.3746/jkfn.2011.40.3.401
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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. DOI:10.1016/j.intimp.2010.12.008 · 2.47 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. DOI:10.3892/ijmm_00000479 · 2.09 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. DOI:10.3858/emm.2010.42.5.038 · 3.45 Impact Factor
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    Sun-Hee Lee · Xiu-Ying Guan · Dae-Ki Kim ·
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    ABSTRACT: mi transcription factor (MITF) is important in regulating the differentiation of mast cells. In particular, MITF regulates the transcription of the mouse mast cell-specific serine protease (mMCP)-6 gene, which is generally expressed by the connective tissue-type of mast cells. In this study, we investigated alternative isoforms of MITF that regulate transcription of the mMCP-6 gene in bone marrow-derived cultured mast cells in mice. The expression of MITF isoforms was examined by RT-PCR. We observed that MITF-A, -E, -H and -Mc were expressed by mucosal-type mast cells cultured in the presence of IL-3, whereas the connective tissue-type mast cells cultured in the presence of stem cell factor (SCF) expressed MITF-A. Overexpression of MITF isoforms increased luciferase activity through the mMCP-6 promoter in NIH-3T3 cells and elevated the level of mMCP-6 expression in the MC/9 mast cell line. Moreover, mMCP-6 expression in mast cells was significantly inhibited by the depletion of MITF. The transcriptional activity and DNA binding of MITF-A was comparable to that of MITF isoforms, including MITF-E, -H, and -Mc. Our results therefore suggest that MITF-A may be an important isoform of MITF in regulating the transcription of mMCP-6 in mouse connective tissue mast cells.
    10/2008; 18(10). DOI:10.5352/JLS.2008.18.10.1348

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