Biomedical subjects

Seung-Heon Hong

Publications and source records attributed to Seung-Heon Hong.

At least 19 recordsLinked to original sources

PubMed2007

Antiapoptotic mechanism of cannabinoid receptor 2 agonist on cisplatin-induced apoptosis in the HEI-OC1 auditory cell line.

Cisplatin is a highly effective chemotherapeutic agent but with significant ototoxic side effects. Apoptosis is an important mechanism of cochlear hair cell loss following exposure to an ototoxic level of cisplatin. The present study investigated the effects of the cannabinoid receptor 2 (CB2) ligand JWH-015 on cisplatin-induced apoptosis. CB2 mRNA was constitutively expressed in the auditory cell line HEI-OC1. By using MTT assay, DNA fragmentation, and FACS analysis, we demonstrated that apoptosis induced by cisplatin was inhibited by treatment with JWH-015 in a dose-dependent manner. Activation of caspase-3, caspase-8, and caspase-9 was detected after treatment with cisplatin, and the cleavage of poly-(ADP)-ribose polymerase (PARP) was observed within cisplatin-treated HEI-OC1 cells. JWH-015 inhibited the activation of caspase-3, caspase-8, and caspase-9; cleavage of PARP; and release of cytochrome c. JWH-015 also inhibited the apoptosis through activation of the extracellular signal-regulated kinase pathway. Finally, JWH-015 inhibited cisplatin-induced reactive oxygen species and tumor necrosis factor-alpha production. Collectively, these findings show that blocking a critical step in apoptosis by using JWH-015 may be a useful strategy to prevent harmful side effects of cisplatin ototoxicity in patients having to undergo chemotherapy.

Analysis of Variance↗

PubMed2006

Epigallocatechin-3-gallate inhibits secretion of TNF-alpha, IL-6 and IL-8 through the attenuation of ERK and NF-kappaB in HMC-1 cells.

BACKGROUND: Epigallocatechin-3-gallate (EGCG) is a major form of tea catechin and has a variety of biological activities. In the present study, we investigated the effect of EGCG on the secretion of TNF-alpha, IL-6 and IL-8, as well as its possible mechanism of action by using the human mast cell line (HMC-1). METHODS: EGCG was treated before the activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187). To investigate the effect of EGCG on PMA+A23187-stimulated HMC-1 cells, ELISA, Western blot analysis, electrophorectic mobility shift assay and luciferase assay were used in this study. RESULTS: EGCG (100 microM) inhibited PMA+A23187-induced TNF-alpha, IL-6 and IL-8 expression and production. EGCG inhibited the intracellular Ca(2+) level. EGCG attenuated PMA+A23187-induced NF-kappaB and extracellular signal-regulated kinase (ERK1/2) activation, but not that of c-Jun N-terminal kinase or p38 mitogen-activated protein kinase. CONCLUSION: EGCG inhibited the production of TNF-alpha, IL-6 and IL-8 through the inhibition of the intracellular Ca(2+) level, and of ERK1/2 and NF-kappaB activation. These results indicate that EGCG may be helpful in regulating mast-cell-mediated allergic inflammatory response.

Calcimycin↗

PubMed2006

Use of scopoletin to inhibit the production of inflammatory cytokines through inhibition of the IkappaB/NF-kappaB signal cascade in the human mast cell line HMC-1.

Scopoletin (6-methoxy-7-hydroxycoumarin) is a coumarin compound and a pharmacologically active agent that has been isolated from several plant species. However, as yet there is no clear explanation of how scopoletin affects the production of inflammatory cytokine. We therefore used cells from the human mast cell line (HMC-1) to investigate this effect. Scopoletin significantly and dose-dependently inhibits the way in which phorbol 12-myristate 13-acetate (PMA) plus A23187 induces the production of inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 (P<0.05). The maximal rates at which scopoletin (0.2 mM) inhibited the production of TNF-alpha, IL-6, and IL-8 were 41.6%+/-4.2%, 71.9%+/-2.5%, and 43.0%+/-5.7%, respectively. In activated HMC-1 cells, the expression level of nuclear factor (NF)-kappaB/Rel A protein was increased in the nucleus whereas the level of NF-kappaB/Rel A in nucleus was decreased by treatment with scopoletin. Scopoletin decreased PMA plus A23187-induced luciferase activity. Scopoletin also inhibits IkappaBalpha phosphorylation and degradation in cytoplasm. These results indicate that scopoletin has a potential regulatory effect on inflammatory reactions that are mediated by mast cells.

Anti-Inflammatory Agents↗

PubMed2006

Oral administration of hot water extracts of Chlorella vulgaris increases physical stamina in mice.

BACKGROUND/AIMS: A unicellular algae, Chlorella vulgaris, was used as a biological response modifier. Although hot water extracts of C. vulgaris (CVE) are thought to augment immune responses, the effect of CVE on fatigue and physical stamina has not been studied. METHODS: In the present study, we investigated the effect of CVE on forced swimming test and blood biochemical parameters related to fatigue, blood urea nitrogen (BUN), creatine kinase (CK), lactic dehydrogenase (LDH), glucose (Glc), and total protein (TP). CVE (0.05-0.15 g/kg/day) was orally administered to mice. RESULTS: After 7 days, the immobility time was decreased in the 0.1- and 0.15-g/kg CVE-treated groups (179 +/- 8.3 and 175 +/- 2.1 s) in comparison with the control group (223 +/- 5.4 s). In addition, the contents of BUN, CK, and LDH in the blood serum were decreased in the CVE-fed group. However, they had no effect on the elevation of Glc and TP level. CONCLUSIONS: The results predict a potential benefit of CVE for enhancing immune function and improving physical stamina.

Administration, Oral↗

PubMed2006

Glechoma hederacea inhibits inflammatory mediator release in IFN-gamma and LPS-stimulated mouse peritoneal macrophages.

Glechoma hederacea (GH) is an herb widely used herb medicine for the treatment of a variety of pathologies. In this study, the effect of GH on interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS)-induced production of nitric oxide (NO), interleukin (IL)-12p70, IL-12p40, tumor necrosis factor-alpha (TNF-alpha), and IL-6 were examined using mouse peritoneal macrophages. GH inhibits IFN-gamma/LPS-induced NO in a dose-dependent manner. The decrease in NO synthesis was reflected as a decreased amount of inducible NO synthase protein. We also found that GH inhibits pro-inflammatory cytokine, IL-12p70, and TNF-alpha production. However, GH increased IFN-gamma/LPS-induced IL-12p40 production. GH doesn't affect the IL-6 production. These findings mean that GH can be used in controlling macrophages mediated inflammation related disease.

Animals↗

PubMed2006

Inhibitory effect of Patrinia scabiosaefolia on acute pancreatitis.

AIM: To investigate the effect of Patrinia scabiosaefolia (PS) on the cholecystokinin (CCK) octapeptide-induced acute pancreatitis (AP) in rats. METHODS: Wistar rats weighing 240-260 g were divided into three groups: (1) Normal saline-treated group; (2) treatment with PS at 100 mg/kg group, in which PS was administered orally, followed by subcutaneous administration of 75 microg/kg CCK octapeptide three times after 1, 3 and 5 h, and this whole procedure was repeated for 5 d; (3) treatment with saline group, in which the protocols were the same as in treatment group with PS. We determined the pancreatic weight/body weight ratio, the levels of pancreatic HSP60, HSP72 and the secretion of pro-inflammatory cytokines. Repeated CCK octapeptide treatment resulted in the typical laboratory findings of experimentally induced pancreatitis. RESULTS: PS reduced the pancreatic weight/body weight ratio, the levels of serum amylase and lipase, and inhibited expressions of pro-inflammatory cytokines in the CCK octapeptide-induced AP. Furthermore, PS pretreatment increased the pancreatic levels of HSP60 and HSP72. CONCLUSION: Pretreatment with PS has an anti-inflammatory effect on CCK octapeptide-induced AP.

Acute Disease↗

PubMed2006

Interleukin-1 receptor antagonist gene polymorphism and traditional classification in obese women.

Cytokines appear to be the major regulators of adipose tissue metabolism. Interleukin- 1 receptor antagonist (IL-1ra) serum levels are increased in human obesity, and are under strong genetic control. The hypothesis was tested that the IL-1ra gene might be a candidate for obesity. Furthermore, the relationship was investigated between Sasang constitution and IL-1ra polymorphism. The frequency of a penta-allelic 86-bp tandem repeat (VNTR) in the intron 2 of IL-1ra gene in 67 lean (BMI<25 kg/m2), 133 overweight (BMI 25-29.9 kg/m2) and 61 obese (BMI>or=30 kg/m2) otherwise healthy Korean subjects was investigated. Total fat mass and percentage body fat were determined by dual-energy X-ray absorptiometry. Subjects were discriminated into four types by QSCC II program as well as clinical data (weight, height, blood pressure, etc.); Teaeumin, Taeyangin, Soyangin, and Soeumin. Genomic DNA was extracted and used for polymerase chain reaction-based genotyping of IL-1ra. The genotypic, or allelic distribution did not differ markedly between the three groups. The relative risk of being obese in comparison with lean was twofold increased in allele 2 carriers, although it was not statistically significant. Carriers of the allele 2 did not show a significant difference in physical and clinical characteristics. However, the relative risk of being obese in comparison with lean was increased in Taeumin subjects (p=.050), and so was in IL-1ra A2- carriers (p=.047). No relationship was found between the IL-1ra polymorphism and BMI in Korean women, but the authors first attempted to find an association among IL-1ra polymorphism, obesity, and Sasang constitution.

Adolescent↗

PubMed2006

Glutathione s-transferase gene polymorphism and ischemic cerebrovascular disease.

Glutathione S-transferase polymorphisms (GST) were examined in 142 cases with ischemic cerebrovascular disease (ICVD) to explore whether the GST polymorphisms confer a risk to an individual to develop ICVD. Tobacco smoke is a major cause of both cancer and vascular disease. The subjects were therefore stratified with ICVD for smoking status, and then the authors examined whether polymorphisms in this detoxification enzyme gene, GST, influence risk of ICVD. The GST genotype was analyzed by the polymerase chain reaction. Neither GSTM1 nor GSTT1 genotypes in the ICVD group was significantly different from the control group (n=344), even in smokers. The authors attempted the combined analysis for GSTM1 and GSTT1 genotypes in ICVD for smoking status. No significant association was observed among the combined genotypes and ICVD. The observations do not confirm the effect of the GSTM1 and GSTT1 genotypes as a risk factor for ICVD, even in smokers. However, this approach provides a way of addressing the hypothesis that environmental genotoxins could play a role in the etiopathogenesis of ICVD.

Adult↗

PubMed2006

The effect of SHJKS on cytokines production and NF-kappaB activation in the peripheral blood mononuclear cells of patients with cerebral infarction.

The Korean genuine medicine "Seonghyangjeongkisan" (SHJKS) has long been used for various cerebrovascular diseases. However, very little scientific investigation has been carried out. Cytokines involved in the regulation of inflammatory reactions and immune responses may play a role in the pathogenesis of cerebral infarction (CI). The aim of the present study is to elucidate how SHJKS modulates the inflammatory reaction in lipopolysaccaride (LPS) plus phytohaemagglutinin (PHA)-stimulated peripheral mononuclear cells (PBMCs) from CI patients. The amount of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-8 in PBMC culture supernatant was significantly increased in the LPS plus PHA treated cells compared to unstimulated cells. SHJKS inhibited the TNF-alpha, IL-1beta, IL-6, and IL-8 production in dose dependent manner. Maximal inhibition rate of the TNF-alpha, IL-1beta, IL-6, and IL-8 by SHJGS (1.0 mg/ml) was 68.01 +/- 0.28% (P < 0.01), 52.11 +/- 0.56 % (P < 0.01), 53.42 +/- 0.46 % (P < 0.01), and 46.70 +/- 0.37% (P < 0.05), respectively. In addition, we show that SHJKS suppressed nuclear factor (NF)-kappaB activation induced by LPS plus PHA, leading to suppression of IkappaB-alpha phosphorylation and degradation. These results suggest that SHJKS might have regulatory effects on LPS plus PHA-induced cytokine production and NF-kappaB activation, which might explain its beneficial effect in the treatment of CI.

Aged↗

PubMed2006

The anti-inflammatory effect of Gigukjiwhangwhangami through the inhibition of nuclear factor-kappaB activation in the peripheral blood mononuclear cells of patients with cerebral infarction.

The Korean genuine medicine "Gigukjiwhangwhangami (GJWGM)" has long been used for various cerebrovascular diseases. However, the exact mechanism that accounts for the anti-inflammatory effect of GJWGM is not completely understood. The aim of the present study is to elucidate how GJWGM modulates the inflammatory reaction in lipopolysaccaride (LPS)-stimulated peripheral mononuclear cells from patients with cerebral infarction. Production of cytokine was measured by the ELISA and RT-PCR method. The level of nuclear factor-kappaB (NF-kappaB)/Rel A protein and NF-kappaB DNA binding activity were determined by the Western blot analysis and TF-EIA method. We showed that GJWGM inhibited the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1alpha, IL-6, and IL-8 induced by LPS in dose dependent manner (p<0.05). Maximal inhibition rate of TNF-alpha, IL-1beta, IL-6 and IL-8 production by GJWGM was about 54.34%, 41.37%, 44.04%, and 54.46%, respectively. GJWGM inhibited the TNF-alpha and IL-8 mRNA expression. In addition, we showed that the inhibitory mechanism of GJWGM is through the suppression of NF-kappaB pathway. Our study suggests that an important molecular mechanism by GJWGM reduce inflammation, which may explain its beneficial effect in the regulation of inflammatory reactions.

Aged↗

PubMed2006

The effect of Panax ginseng on forced immobility time & immune function in mice.

BACKGROUND & OBJECTIVES: Panax ginseng has been used as a traditional medicine for many years mainly among Asian peoples for developing physical strength. We undertook this study to determine the immune-enhancement effect of P. ginseng using a forced swimming test (FST) and by measuring cytokine production in MOLT-4 cell culture and mouse peritoneal macrophages. METHODS: P. ginseng was orally administered to mice once a day for 7 days. The anti-immobility effect of P. ginseng on the FST and blood biochemical parameters related to fatigue, glucose (Glc); blood urea nitrogen (BUN); latic dehydrogenase (LDH); total protein (TP) and production of cytokines in human T cell line, MOLT-4 cells and mouse peritoneal macrophages were investigated. RESULTS: After two and seven days, the immobility time was decreased in the P. ginsengadministrated mice as compared to the control group; however, this reduction was not significant. In addition, the amount of TP in the blood serum was significantly increased. However, the levels of Glc, BUN, and LDH did not show a significant change. P. ginseng significantly (P<0.05) increased interferon (IFN)-gamma production and expression as compared to control at 48 h in MOLT-4 cells. P. ginseng plus recombinant IFN-gamma instead of P. ginseng alone significantly increased the production of the tumour necrosis factor (TNF)-alpha in the mouse peritoneal macrophages. INTERPRETATION & CONCLUSION: Our results suggest that P. ginseng may be useful for an immune promoter. Further studies are needed to understand the mechanism of its action.

Adjuvants, Immunologic↗

PubMed2005

Involvement of mitogen-activated protein kinase and NF-kappaB activation in Ca2+-induced IL-8 production in human mast cells.

Interleukin-8 (IL-8) is a potent proinflammatory chemokine that plays an important role in inflammation by activating and recruiting neutrophils, lymphocytes, and eosinophils. To demonstrate the effect of intracellular Ca(2+) on IL-8 production and related signaling, we stimulated human mast cell line HMC-1 with either calcium ionophore A23187 or thapsigargin. Increase of intracellular Ca(2+) resulted in inducing IL-8 gene expression and protein secretion, and addition of EGTA or BAPTA/AM before Ca(2+) stimulation inhibited the induction of IL-8 production. Intracellular Ca(2+) triggered the activation of mitogen-activated protein kinase (MAPK) in HMC-1, especially p42 and p44 isoforms of extracellular signal-regulated kinase (ERK) and p38 MAPK, but not c-Jun N-terminal kinase (JNK). Pretreatment of MAPK inhibitors (PD98059 and SB203580) markedly blocked Ca(2+)-induced IL-8 production from cells, and anti-inflammatory drugs, such as dexamethasone and cyclosporin A, partially inhibited the activation of ERK1/2. We determined that increased Ca(2+) activates the nuclear translocation of the transcription factor NF-kappaB. NF-kappaB inhibitors blocked the ability of Ca(2+) to induce IL-8 production, and the activation of NF-kappaB was required for intracellular Ca(2+)-induced up-regulation of IL-8. These results suggest that increased intracellular Ca(2+) stimulated p38 and ERK1/2 MAPK signaling cascades result in NF-kappaB activation and IL-8 production in HMC-1 cells. This study is the first to identify the intracellular signaling pathways involved in the Ca(2+)-mediated up-regulation of IL-8 synthesis and release from HMC-1 cells.

Calcimycin↗

PubMed2005

Sopoongsan inhibits mast cell-mediated anaphylactic reactions and inflammatory cytokine secretion.

BACKGROUND: Mast cells are key effector cells in the early-phase allergic inflammation and in diverse immunological and pathological processes. Sopoongsan (SPS), a traditional Korean medicine, has been used as therapeutics for allergic diseases such as atopic dermatitis (AD). The precise effect in experimental models of SPS, however, remains unknown. In this report, we investigated the effect of SPS on mast cell-mediated anaphylactic reactions and cytokine production in in vivo and in vitro murine models. METHODS: Compound 48/80-induced histamine and ear swelling were measured with the various concentrations of SPS. The amount of dye was determined colorimetrically after antidinitrophenyl IgE antibody-induced passive cutaneous anaphylaxis reaction. Secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and IL-6 in supernatants from HMC-1 cells was measured by a sandwich enzyme-linked immunosorbent assay. The expression level of nuclear factor (NF)-kappaB/Rel A in the nucleus and the activation of mitogen-activated protein kinases (MAPKs) were examined by Western blot analysis. RESULTS: SPS inhibited the degranulation and histamine release from the rat peritoneal mast cells activated by compound 48/80. Compound 48/80-induced ear swelling was significantly reduced. SPS also showed an inhibitory effect of passive cutaneous anaphylaxis reaction. Significantly reduced levels (p < 0.05) of TNF-alpha, IL-8 and IL-6 were observed in the human mast cell line with SPS and SPS components. In addition, SPS inhibited an increase of NF-kappaB and extracellular signal-regulated kinase 1/2 activity. CONCLUSIONS: These findings suggest that SPS has an inhibitory effect on atopic allergic reaction and this might be useful for the clinical application to treat allergic diseases such as AD.

Administration, Oral↗

PubMed2005

The immunosuppressive effect of Buchang-tang through inhibition of mitogen-activated protein kinase and nuclear factor activation in MOLT-4 cells.

Buchang-tang (BCT) has been known to suppress inflammatory and autoimmune responses. Accordingly, BCT has been clinically used in Korea as an immunomodulatory oriental medicine. Here, we report on the mechanism of action of BCT in activated MOLT-4 cells by determining the affected signaling pathways. BCT inhibits extracellular signal-regulated kinases (ERK)l/2 and p38 activation but does not interfere with phosphorylation of other mitogen-activated protein kinases, c-Jun NH2-terminal kinases 1/2 in MOLT-4 cells. The nuclear localization of nuclear factor of activated T cells 2 (NFATc) was blocked by BCT. Also, degradation of inhibitor kappaB-alpha and transactivation by nuclear factor-kappa B (NF-kappaB)/Rel A were impaired. Furthermore, interlukin (IL)-2 mRNA and protein levels were significantly diminished by BCT treatment. Our data indicate that BCT inhibits ERK1/2, p38 activation, nuclear translocation of NFATc, and NF-kappaB, resulting in diminished secretion of IL-2.

Active Transport, Cell Nucleus↗

PubMed2005

Gamibojungikki-tang decreases immobility time on the forced swimming test and increases interferon-gamma production from MOLT-4 cells.

Gamibojungikki-tang (GBIT) has been used for the purpose of development of physical strength in Korea. We investigated the anti-immobility effect of GBIT on the forced swimming test (FST) and then measured the blood biochemical parameters related to fatigue, glucose (Glc); blood urea nitrogen (BUN); lactic dehydrogenase (LDH); creatine kinase (CK) and total protein (TP). GBIT (0.01, 0.1, 1 g/kg) was orally administered to mice for 7 days. After 7 days, the immobility time was significantly decreased in the GBIT-administration group (105.0+/-12.1 s for 1 g/kg) in comparison with the control group (152.3+/-16.2 s). The contents of Glc and TP in the blood serum were significantly increased in GBIT-administration group (1g/kg) compared with control group, while LDH was significantly decreased. Surface phenotyping of spleen cells by FACS analysis revealed an increasing tendency of CD4+ and CD8+ number, without statistical significance. In addition, GBIT (0.01-1 mg/ml) increased the interferon-gamma and interlukin-2 levels in MOLT-4 T-cells. These results suggest that GBIT may be useful in the immune function improvement.

Animals↗

PubMed2005

Regulatory effect of atopic allergic reaction by Carpopeltis affinis.

Carpopeltis affinis Okamura (CA, Halymeniaceae) has long been used as therapeutics for various allergic diseases in Korea. The precise effects of CA in experimental models, however, have remained unknown. We studied the effects of a methanol extract of CA on atopic allergic reaction. Histamine content was measured by the o-phthalaldehyde spectrofluorometric procedure. Cytokines were measured by a modified enzyme-linked immunosorbent assay. Cytotoxicity was determined by the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. CA significantly inhibited the histamine release and beta-hexosaminidase release from rat peritoneal mast cells. CA also inhibited interleukin-8 and tumor necrosis factor-alpha secretion from the phorbol 12-myristate 13-acetate and A23187-induced HMC-1 cells (human mast cell line). 48 h exposure to CA (1.0, 10, and 100 microg/ml) had little effect on HMC-1 cell viability. Our results suggest that CA has an inhibitory effect on mast cell-dependent allergic reaction and thus may be useful in the treatment of atopic dermatitis.

Animals↗

PubMed2005

Ethanol induces the production of cytokines via the Ca2+, MAP kinase, HIF-1alpha, and NF-kappaB pathway.

In the present study, we sought to investigate the signal transduction pathways of expression of cytokines in the ethanol-stimulated human mast cell line, HMC-1. Ethanol significantly increased the intracellular calcium level in HMC-1. Ethanol also significantly enhanced IL-6, TNF-alpha, and TGF-beta1 production compared with media control, but did not significantly affect the IL-1beta production. After 8 h of stimulation, ethanol increased mRNA and protein expression levels of TNF-alpha and TGF-beta1 in HMC-1. The increased cytokine level was significantly inhibited by BAPTA-AM, PD98059, and SB203580. These inhibitors also inhibited ethanol-induced ERK and p38 MAPK phosphorylation. Ethanol resulted in a great increase in protein levels and promoter activity driving luciferase expression of HIF-1alpha and NF-kappaB in HMC-1 cells, but it did not affect on HIF-1alpha mRNA expression. Our observations show that calcium, MAPK activation, HIF-1alpha, and NF-kappaB are necessary for ethanol-induced TNF-alpha and TGF-beta1 expression. These results may have important implications for the study of alcohol-related diseases.

Blotting, Western↗

PubMed2005

Inhibitory effects of Okbyungpoong-Gamhmi on anaphylactic responses.

We investigated the effect of a herbal formulation Okbyungpoong-Gamhmi (OG) on mast cell-dependent anaphylactic reactions by intra-rectal administration. OG concentration dependently inhibited compound 48/80-induced anaphylaxis-like response and ear swelling response with doses of 0.01-1g/kg. OG also inhibited the passive cutaneous anaphylaxis at the same concentrations. The histamine release induced by compound 48/80 or IgE from the rat peritoneal mast cells was reduced by 64.2 and 63.6%, respectively, at 1g/l. These results provide evidence that intra-rectal therapy of OG may be beneficial in the treatment of anaphylactic response.

Anaphylaxis↗