Min Sung Lee

Soonchunhyang University, Onyang, Chungcheongnam-do, South Korea

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Publications (14)32.05 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Caffeoyl derivatives exhibit antiinflammatory and antioxidant effects. However, the effect of 3,4,5-tricaffeoylquinic acid on the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in keratinocytes that may be involved in skin diseases has not been studied. In this respect, we investigated the effect of 3,4,5-tricaffeoylquinic acid on TRAIL-induced apoptosis in human keratinocytes. 3,4,5-Tricaffeoylquinic acid and oxidant scavengers attenuated the decrease in the cytosolic levels of Bid, Bcl-2, and survivin proteins; the increase in the levels of cytosolic Bax, p53, and phosphorylated p53; the increase in the levels of phosphorylated p38; the increase in the mitochondrial levels of the voltage-dependent anion channel; loss of the mitochondrial transmembrane potential; the release of cytochrome c; activation of caspases (8, 9, and 3); cleavage of poly [ADP-ribose] polymerase-1; production of reactive oxygen species; the depletion of glutathione (GSH); nuclear damage; and cell death in keratinocytes treated with TRAIL. These results suggest that 3,4,5-tricaffeoylquinic acid may reduce TRAIL-induced apoptosis in human keratinocytes by suppressing the activation of the caspase-8 and Bid pathways and the mitochondria-mediated cell death pathway. The effect appears to be associated with the inhibitory effect on the production of reactive oxygen species and depletion of GSH. 3,4,5-Tricaffeoylquinic acid appears to be effective in the prevention of TRAIL-induced apoptosis-mediated skin diseases. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.
    Phytotherapy Research 07/2015; DOI:10.1002/ptr.5425 · 2.40 Impact Factor
  • Yoon Jeong Nam · Da Hee Lee · Min Sung Lee · Chung Soo Lee
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    ABSTRACT: Dysfunction of the proteasome system has been suggested to be implicated in neuronal degeneration. Modulation of KATP channels appears to affect the viability of neuronal cells exposed to toxic insults. However, the effect of KATP channel blockers on the neuronal cell death mediated by proteasome inhibition has not been studied. The present study investigated the effect of KATP channel blockers on proteasome inhibitor-induced apoptosis in differentiated PC12 cells and SH-SY5Y cells. 5-Hydroxydecanoate (a selective KATP channel blocker) and glibenclamide (a cell surface and mitochondrial KATP channel inhibitor) reduced the proteasome inhibitor-induced apoptosis. Addition of the KATP channel blockers attenuated the proteasome inhibitor-induced changes in the levels of apoptosis-related proteins, the loss of the mitochondrial transmembrane potential, the increase in the formation of reactive oxygen species and the depletion of glutathione in both cell lines. The results show that KATP channel blockers may attenuate proteasome inhibitor-induced apoptosis in PC12 cells by suppressing activation of the mitochondrial pathway and of the caspase-8- and Bid-dependent pathways. The preventive effect appears to be associated with the inhibition of the formation of reactive oxygen species and the depletion of glutathione. KATP channel blockade appears to prevent proteasome inhibition-induced neuronal cell death. Copyright © 2015. Published by Elsevier B.V.
    European journal of pharmacology 07/2015; 764. DOI:10.1016/j.ejphar.2015.06.049 · 2.68 Impact Factor
  • Yoon Jeong Nam · Da Hee Lee · Min Sung Lee · Chung Soo Lee
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    ABSTRACT: Microbial product lipopolysaccharide has been shown to be involved in the pathogenesis of inflammatory skin diseases. Parthenolide present in extracts of the herb feverfew has demonstrated an anti-inflammatory effect. However, the effect of parthenolide on the Akt/mTOR and NF-κB pathway activation-induced productions of inflammatory mediators in keratinocytes has not been studied. Using human keratinocytes, we investigated the effect of parthenolide on the inflammatory mediator production in relation to the Toll-like receptor-4-mediated-Akt/mTOR and NF-κB pathways, which regulate the transcription genes involved in immune and inflammatory responses. Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1β and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-κB in keratinocytes. The results show that parthenolide appears to attenuate the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor-4-mediated activation of the Akt, mTOR, and NF-κB pathways. The activation of signaling transduction pathways appear to be regulated by reactive oxygen species. Parthenolide appears to attenuate the microbial product-mediated inflammatory skin diseases.
    Archiv für Experimentelle Pathologie und Pharmakologie 05/2015; DOI:10.1007/s00210-015-1132-3 · 2.36 Impact Factor
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    ABSTRACT: The extract of from the barks of Ilex Rotunda Thunb has demonstrated anti-inflammatory and anti-oxidant effects. Nevertheless, the effect of rotundarpene (4-caffeoyl-3-methyl-but-2-ene-1,4-diol) on the neuronal cell death induced by cholesterol oxidation products is unclear. We assessed the preventive effect of rotundarpene on the cholesterol oxidation product-induced apoptosis in neuronal cells using differentiated PC12 cells. 7-Ketocholesterol and 25-hydroxycholesterol induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, increase in Bax levels, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and an increase in the tumor suppressor p53 levels. Rotundarpene attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. The results show that rotundarpene may attenuate the cholesterol oxidation product-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect appears to be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH. Rotundarpene appears to attenuate cholesterol-oxidation product-mediated neuronal degeneration. Copyright © 2015. Published by Elsevier B.V.
    European Journal of Pharmacology 01/2015; 749. DOI:10.1016/j.ejphar.2014.11.048 · 2.68 Impact Factor
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    ABSTRACT: The dysfunction of the proteasome system is suggested to be implicated in neuronal degeneration. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. However, the effect of 3,4,5-tricaffeoylquinic acid on the neuronal cell death induced by proteasome inhibition has not been studied. Therefore, in the respect of cell death process, we assessed the effect of 3,4,5-tricaffeoylquinic acid on the proteasome inhibition-induced programmed cell death using differentiated PC12 cells. The proteasome inhibitors MG132 and MG115 induced a decrease in Bid, Bcl-2, and survivin protein levels, an increase in Bax, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), and an increase in the tumor suppressor p53 levels. Treatment with 3,4,5-tricaffeoylquinic acid attenuated the proteasome inhibitor-induced changes in the programmed cell death-related protein levels, formation of reactive oxygen species, GSH depletion and cell death. The results show that 3,4,5-tricaffeoylquinic acid may attenuate the proteasome inhibitor-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect of 3,4,5-tricaffeoylquinic acid appears to be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
    Neurochemical Research 05/2014; 39(8). DOI:10.1007/s11064-014-1327-x · 2.55 Impact Factor
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    ABSTRACT: Microbial components have been shown to be involved in the pathogenesis of inflammatory skin diseases. The extract of from the barks of Ilex rotunda Thunb has demonstrated anti-inflammatory and anti-oxidant effects. However, the effect of hemiterpene rotundarpene (4-caffeoyl-3-methyl-but-2-ene-1,4-diol) on the Toll-like receptor (TLR)-2 activation-induced production of inflammatory mediators in keratinocytes has not been studied. Using human keratinocytes, we investigated the effect of rotundarpene on the inflammatory mediator production in relation to the TLR-2-mediated-Akt and NF-κB pathways, which regulates the transcription genes involved in immune and inflammatory responses. Rotundarpene, Akt inhibitor, Bay 11-7085 and N-acetylcysteine each attenuated the lipoteichoic acid- or peptidoglycan-induced production of cytokines and chemokines, expression of TLR-2, activation of NF-κB and Akt, and formation of reactive oxygen species in keratinocytes. Cyclosporine A attenuated the bacterial component-induced production of inflammatory mediators but did not reduce the formation of reactive oxygen species. The results show that rotundarpene may attenuate the bacterial component-stimulated production of inflammatory mediators in keratinocytes by suppressing the TLR-2-mediated activation of the Akt and NF-κB pathways. The effect of rotundarpene may be attributed to its inhibitory effect on the formation of reactive oxygen species. Rotundarpene may exert a preventive effect against the bacterial component-mediated inflammatory skin diseases.
    International immunopharmacology 12/2013; 18(2). DOI:10.1016/j.intimp.2013.12.016 · 2.71 Impact Factor
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    ABSTRACT: Quercetin and its derivatives have anti-inflammatory and anti-oxidant effects. However, the effect of quercetin-3-O-(2″-galloyl)-α-l-rhamnopyranoside (QGR), a new quercetin derivative, on the tumor necrosis factor (TNF)-α-stimulated production of inflammatory mediators in keratinocytes is unclear. In addition, the effect of QGR on the ERK and NF-κB-mediated inflammatory process has not been studied. In human keratinocyte HaCat cells, we investigated the effect of QGR on the TNF-α-stimulated production of inflammatory mediators in relation to the nuclear factor (NF)-κB, which regulates the transcription genes involved in immune and inflammatory responses. QGR inhibited the TNF-α-stimulated production of cytokines and chemokines in HaCaT cells. QGR, dexamethasone, cyclosporine A, Bay 11-7085 (an inhibitor of NF-κB activation) and cell signaling ERK inhibitor attenuated the TNF-α-induced formation of inflammatory mediators and activation of the NF-κB and ERK. Unlike other compounds, dexamethasone and cyclosporine A did not reduce formation of reactive oxygen species. The results show that QGR may attenuate TNF-α-stimulated inflammatory mediator production in HaCaT cells by suppressing the activation of the ERK-mediated NF-κB pathway that is mediated by reactive oxygen species. Additionally, QGR may exhibit a preventive effect against the proinflammatory mediator-induced skin diseases by inhibiting the activation of the ERK and NF-κB pathways.
    International immunopharmacology 05/2013; 16(4). DOI:10.1016/j.intimp.2013.05.001 · 2.71 Impact Factor
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    ABSTRACT: Study Type – Prognosis (cohort) Level of Evidence 2b What's known on the subject? and What does the study add? The second to fourth digit ratio (hereafter the digit ratio) of the right hand is related to the activity of the androgen receptor. Five α-reductase inhibitor (5ARI) reduces the prostate volume of patients with BPH. In terms of prostate volume reduction, large-scale placebo-controlled studies show that patients with BPH do not always respond well to 5ARI treatment. Patients with a higher digit ratio respond well to dutasteride treatment compared to those with a lower digit ratio. These results suggest that the digit ratio might be a predictor of the response to dutasteride treatment.
    BJU International 07/2012; 110(11C). DOI:10.1111/j.1464-410X.2012.11343.x · 3.13 Impact Factor
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    ABSTRACT: Natural phenol licorice compounds have been shown to induce apoptosis in cancer cells. 3-(5'-Hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1) may enhance the sensitivity of cancer cells to anticancer drugs. However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells has not been studied. We assessed the combined effect of licochalcone A and YC-1 on apoptosis in human epithelial ovarian carcinoma cell lines in relation to the cell death process. In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels. YC-1 enhanced licochalcone A-induced apoptosis-related protein activation, nuclear damage and cell death. These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The combination of licochalcone A and YC-1 may confer a benefit in the treatment of human epithelial ovarian adenocarcinoma.
    European journal of pharmacology 03/2012; 683(1-3):54-62. DOI:10.1016/j.ejphar.2012.03.024 · 2.68 Impact Factor
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    ABSTRACT: Microbial products, including lipopolysaccharide, may be involved in the pathogenesis of skin diseases such as atopic dermatitis. Diarylheptanoids such as oregonin and hirsutenone have been shown to have an anti-inflammatory effect. We investigated the effect of hirsutenone on lipopolysaccharide-induced inflammatory mediator production in keratinocytes in relation to the Toll-like receptor 4-mediated activation of the extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-kappaB pathways. Hirsutenone, dexamethasone, ERK inhibitor or Bay 11-7085 (an inhibitor of NF-kappaB activation) reduced the lipopolysaccharide-induced production of cytokines IL-1beta and IL-8, and the chemokine CCL17. Hirsutenone, ERK inhibitor or Bay 11-7085 also prevented the lipopolysaccharide-induced expression of Toll-like receptor 4, the phosphorylation of inhibitory kappaB-alpha, the activation of NF-kappaB and the expression of ERK. The results show that hirsutenone may reduce the lipopolysaccharide-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated NF-kappaB activation that is regulated by the ERK pathway. These findings suggest that hirsutenone may exert a preventive effect against microbial endotoxin lipopolysaccharide-induced inflammatory skin diseases through inhibition of ERK pathway-mediated NF-kappaB activation.
    International immunopharmacology 02/2010; 10(4):520-5. DOI:10.1016/j.intimp.2010.01.015 · 2.71 Impact Factor
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    ABSTRACT: Dendritic cell (DC)-based tumor vaccine is an attractive modality for the treatment of hormone-refractory prostate cancer (HRPC) because it has some efficacy and few side effects in patients with poor general conditions. The aim of this study was to establish which is the most effective DC vaccine for the treatment of HRPC. We compared DC vaccine sensitized with tumor lysate and a fusion vaccine of DCs and tumor cells. The DU145 cancer cell line was purchased from the American Type Culture Collection. DCs were cultured from peripheral blood monocytes. Peripheral blood monocytes were cultured in RPMI 1640 medium supplemented with interleukin-4 (IL-4), granulocyte-macrophage colony-stimulating factor, and 10% fetal calf serum. Tumor necrosis factor-alpha was added on day 7 to support maturation. Functional activity was measured in three groups: the DC single-culture group, the DC culture group with DC vaccine sensitized with tumor lysates, and the DC culture group prepared with tumor fusion vaccine made from irradiated tumor cells and monocyte-derived DCs by the polyethylene glycol method. By FACS analysis, the rate of DC-tumor fusion vaccine was 20.3+/-3%. The IL-12 level produced by the DC-tumor fusion vaccine was significantly higher than that of DCs pulsed with tumor lysate (p<0.05). Also, the generation of interferon-gamma by tumor-specific T cells in the DC-tumor fusion vaccine group was superior to that of DCs pulsed with tumor lysate (p<0.05). In addition, the T cells of the tumor lysate-pulsed DCs and tumor fusion vaccine had 1.6 and 2.5 times the functional activity, respectively, of the DC single-culture group in killing tumor cells in the cytotoxicity assay. The DC-tumor fusion vaccine seems to be more effective than DC single-culture or DC-tumor lysate vaccine in the treatment of HRPC.
    Korean journal of urology 02/2010; 51(2):139-44. DOI:10.4111/kju.2010.51.2.139
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    ABSTRACT: Defects in mitochondrial function have been shown to participate in the induction of cell death in cancer cells. The present study was designed to assess the toxic effect of 18beta-glycyrrhetinic acid against human cervix and uterus tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18beta-glycyrrhetinic acid and anti-cancer drugs. 18beta-Glycyrrhetinic acid induced the nuclear damage, changes in the mitochondrial membrane permeability, formation of reactive oxygen species and depletion of glutathione in SiHa cells. It caused cell death by inducing the increase in the pro-apoptotic Bax protein and cytochrome c levels, reduction in anti-apoptotic Bcl-2 level, subsequent caspase-3 activation and loss of the mitochondrial transmembrane potential. Unlike 18beta-glycyrrhetinic acid, a pro-compound glycyrrhizin up to 100 microM did not induce cell death and depletion of glutathione. Combined treatment of mitomycin c (or doxorubicin) and 18beta-glycyrrhetinic acid revealed a synergistic toxic effect. Meanwhile, combination of camptothecin and 18beta-glycyrrhetinic acid exhibited an additive cytotoxic effect. Results suggest that 18beta-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation. The effect may be associated with increased formation of reactive oxygen species and depletion of glutathione. Combined treatment of antibiotic anti-cancer drug and 18beta-glycyrrhetinic acid seems to exhibit a synergistic toxic effect.
    Life Sciences 09/2008; 83(13-14):481-9. DOI:10.1016/j.lfs.2008.07.014 · 2.30 Impact Factor
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    ABSTRACT: To assess testicular rupture, scrotal haematoma, penile fracture and penile injury, comparing the prognoses of surgery and conservative management, as trauma to male external genital organs can cause devastating effects on patients and their partners. We reviewed the medical records of 156 male patients who presented to our emergency centre with trauma to the external genital organs between January 1996 and March 2006. In all, 74 patients had testicular rupture, 32 penile fracture, 26 a penile injury and 24 a scrotal haematoma (mean age 27.8 years). The main cause of trauma was assault (52, 33%). Four of 14 patients with penile trauma who were managed conservatively had complications. Of 20 patients, 17 had a partial orchidectomy and were followed for a month after surgery; scrotal ultrasonography showed three cases of testicular atrophy. The mean hospital stay was less for patients with surgical intervention, at 6.4 days, than for those managed conservatively, at 8.7 days (P < 0.05). A visual analogue pain scale showed less pain in patients who were surgically treated (P < 0.05). Prompt surgical intervention is crucial; it should be considered by urologists, and is strongly recommended. Ultrasonography was highly sensitive and specific, and should be used in all patients with trauma to the external genital organs, to aid diagnosis and evaluation before surgery.
    BJU International 01/2008; 101(2):211-5. DOI:10.1111/j.1464-410X.2007.07265.x · 3.13 Impact Factor
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    ABSTRACT: Canal transobturator tape (TOT) was developed to reduce the complications of TOT by modifying the sling procedure of TOT with using a distal urethral polypropylene sling (DUPS). The aim of this present study was to describe a modified surgical technique for the treatment of female urodynamic stress urinary incontinence and to assess the objective and subjective efficacy of Canal TOT.
    Korean Journal of Urology 01/2008; 49(12). DOI:10.4111/kju.2008.49.12.1119

Publication Stats

104 Citations
32.05 Total Impact Points

Institutions

  • 2008–2015
    • Soonchunhyang University
      • College of Medicine
      Onyang, Chungcheongnam-do, South Korea
  • 2012
    • Chung-Ang University
      • College of Medicine
      Sŏul, Seoul, South Korea
  • 2008–2010
    • Gachon University
      • Department of Urology
      Seongnam, Gyeonggi, South Korea