• Journal of Ginseng Research
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• 제35권4호
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• pp.479-486
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• 2011

Atopic dermatitis (AD) is an allergic, inflammatory skin disease characterized by chronic eczema and mechanical injury to the skin, caused by scratching. Korean red ginseng (RG) has diverse biological activities, but the molecular effects of RG on allergic diseases, like AD, are unclear. The present study was designed to investigate whether RG inhibits 1-chloro-2,4-dinitrobenzene (DNCB)-induced AD in a mouse model. DNCB was applied topically on the dorsal surface of Balb/c mice to induce AD-like skin lesions. We observed the scratching behavior and examined the serum IgE level and interleukin (IL)-4 and IL-10 in splenocytes compared with dexamethasone. We also evaluated the DNCB-induced mitogen-activated protein kinases (MAPKs), NF-${\kappa}B$, and Ikaros activities after RG treatment using reverse transcriptase-polymerase chain reaction, Western blotting, and ELISA. Our data showed that the topical application of RG significantly improved the AD-like skin lesions and scratching behavior. RG decreased not only the mRNA expression of IL-4 and IL-10, but also the secretion of IL-4 protein and serum IgE in mice. Additionally, RG treatment decreased the DNCB-induced MAPKs activity and subsequent Ikaros translocation irrespective of NF-${\kappa}B$. We suggest that RG may be useful as a therapeutic nutrition for the treatment of AD.

• 동의신경정신과학회지
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• 제20권1호
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• pp.177-197
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• 2009

Objectives : Gliosis disturbs recovery of damaged astrocytes following central nervous system(CNS) injury. Gliosis relates to up-regulation of CD81 and GFAP. In glial cells at injured CNS, the expression of CD81 and GFAP is increased. It is possible that when the gliosis formation is suppressed, regeneration of oxons can occur. According to the recent study, the treatment with anti CD81 antibodies enhanced functional recovery in rats with spinal injury. So, the author studies the effect of water extract of Radix Ginseng on regulation of CD81 and GFAP with CNS injury. Methods : In the cell study, hypoxic damage was induced by CoC12. And according to Longa et al, cerebral ischemia was made by middle cerebral artery occlusion in the rat. Cross sections of rat brain were examined under microscope. MTT analysis was performed to examine cell viability, cell based ELISA, Western Blot and PCR were used to detect the expression of CD81 and GFAP. Results : The following results were obtained. 1. We found that CD81 and GFAP were decreased in hypoxic injured cells following Radix Ginseng administration. 2. We injected the extract of Radix Ginseng to the middle cerebral artery occlusion in rats, and the immunohistochemistry analysis showed that CDS1 and GFAP were decreased. Conclusions : These results show that the extract of Radix Ginseng could suppress the gliosis formation and prevent cell death, by controlling the expression of CDS1 and GFAP. Therefore, Radix Ginseng could be a useful to regenerate CNS injury.

• 대한미생물학회지
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• 제35권1호
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• pp.41-48
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• 2000

Bacteroides fragilis and Escherichia coli, normal colonic inhabitants, are the most frequently isolated bacteria in infected tissues, particularly in intraabdominal abscesses. This study was designed to determine whether enteric bacteria may alter the B. fragilis-induced expression of pro inflammatory cytokines in mouse peritoneal tissue (MPT). After C57BL/6 mice were inoculated with abscess-forming mixture containing B. fragilis in the presence or absence of E. coli, RNA was extracted from MPT. Expression of interleukin (IL)-$1{\alpha}$ and tumor necrosis factor $(TNF){\alpha}$ mRNA was assessed using RT-PCR and standard RNA. Each cytokine protein was also measured by ELISA. The co-inoculation of E. coli into mouse peritoneal cavity advanced the onset of abscess development by B. fragilis infection. When mouse was co-infected with E. coli and B. fragilis intraperitoneally, there was a synergistic increase in the expression of IL-$1{\alpha}$ and $TNF{\alpha}$ mRNA in MPT and this was paralleled by increased cytokine protein secretion. Mixed inoculation of heat-killed E. coli and B. fragilis did not cause a synergistic increase in those cytokine mRNA expression. These results suggest that enteric bacteria may significantly affect proinflammatory cytokine signal produced by host peritoneal cavity in response to B. fragilis infection.

• BMB Reports
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• 제33권1호
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• pp.92-95
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• 2000

The HIV-1 p24(202-221) sequence ETINNEEEWDRVHPV HAGP contains a B-cell epitope with the earliest immune response and the highest antibody titer against anti-mouse sera obtained by immunization with p24 antigens. A novel mouse monoclonal antibody (mAb) was generated against the immunodominant B-cell epitope of the HIV-1 p24 capsid protein, p24(202-221). BALB/c mice were immunized with the four branched multiple antigenic peptide (MAP) containing the HIV-1p24(202-221) sequence, and antibody-secreting hybridoma were produced by fusion of mouse splenocytes with P3X63Ag8.653, mouse myeloma cells. One clone which produced the antigen-specific mAb named KI-24 (Isotype IgG1, light chain: ${\kappa}$) was identified. mAb KI-24 was highly specific for both the p24(202-221) and p24 proteins when analyzed by ELISA and Western blotting. Since p24(202-221) also contains a cytotoxic T-lymphocyte epitope, this specfic peptide epitope and the monoclonal antibody with specific reactivity against the p24 protein and p24(202-221) can be used in peptide vaccine development and p24 antigen detection from HIV patients.

• Nutrition Research and Practice
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• 제10권3호
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• pp.251-258
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• 2016

BACKGROUND/OBJECTIVES: Several pharmacological properties of red rice extract have been reported including anti-oxidant, anti-tumor, and reduced cancer cell invasion. This study was conducted to evaluate the anti-inflammatory effects of red rice extract on the production of inflammatory mediators in lipopolysaccharide (LPS)-induced Raw 264.7 macrophages. MATERIALS/METHODS: Pro-inflammatory cytokines including tumor necrosis factor-${\alpha}$ and interleukin-6 were determined by ELISA and cyclooxygenase-2 and inducible nitric oxide synthase expression was evaluated using western blot analysis. In addition, the signaling pathway controlling the inflammatory cascade such as nuclear factor kappa B ($NF-{\kappa}B$), activator proteins-1 (AP-1), and mitogen-activated protein kinase (MAPK) was determined. RESULTS: Our results showed that red rice polar extract fraction (RR-P), but not non-polar extract fraction, inhibited interleukin-6, tumor necrosis factor-${\alpha}$, and nitric oxide production in LPS-induced Raw 264.7 cells. RR-P also reduced the expression of inflammatory enzymes, inducible nitric oxide synthase, and cyclooxygenase-2. In addition, activation of AP-1 and $NF-{\kappa}B$ transcription factor in the nucleus was abrogated by RR-P. RR-P inhibited the phosphorylation of extracellular signaling-regulated kinase 1/2, c-Jun NH2-terminal kinase, and p38 MAPK signaling responsible for the expression of inflammatory mediators in LPS-stimulated Raw 264.7 cells. Based on chemical analysis, high amounts of proanthocyanidin and catechins were detected in the RR-P fraction. However, only proanthocyanidin reduced $NF-{\kappa}B$ and AP-1 activation in LPS-activated Raw 264.7 cells. CONCLUSION: These observations suggest that the anti-inflammatory properties of RR-P may stem from the inhibition of pro-inflammatory mediators via suppression of the AP-1, $NF-{\kappa}B$, and MAPKs pathways.

• Reproductive and Developmental Biology
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• 제35권2호
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• pp.143-149
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• 2011

Arthritis is a common disease in aged people, and is clinically divided into rheumatoid arthritis (RA) and osteoarthritis (OA). Although common symptoms such as pain are present, the underlying pathological mechanisms are slightly different. Therefore, the objectives of the present study were to compare joint damage induced by RA and OA by analyzing the major morphological and molecular differences, and to propose a suitable therapeutic intervention based on the pathophysiological conditions of bones and joints. For the RA animal model, 8-week-old DBA1/J mice were immunized with bovine type II collagen emulsified in complete Freund's adjuvant (CFA). Normal C57BL/6 mice (over 2 years of age) were used for OA. The clinical arthritis score was calculated using a subjective scoring system, and paw thicknesses were measured using calipers. The serum TNF ${\alpha}$ level was analyzed using an ELISA kit. Micro-CT was used to identify pathological characteristics and morphological changes. In collagen-induced RA mice, there were increased ankle joint volumes and clinical scores (p<0.01). The concentration of TNF ${\alpha}$ was significantly increased from 3 to 7 weeks after immunization. Micro-CT images showed trabecular bone destruction, pannus formation, and subchondral region destruction in RA mice. OA among aged mice showed narrowed joint spaces and breakdown of articular cartilage. This study suggests that a careful therapeutic intervention between RA and OA is required, and it should be based on morphological alteration of bone and joint.

• Nutrition Research and Practice
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• 제10권6호
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• pp.623-628
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• 2016

BACKGROUND/OBJECTIVES: Obesity-induced steatohepatitis accompanied by activated hepatic macrophages/Kupffer cells facilitates the progression of hepatic fibrinogenesis and exacerbates metabolic derangements such as insulin resistance. Heme oxyganase-1 (HO-1) modulates tissue macrophage phenotypes and thus is implicated in protection against inflammatory diseases. Here, we show that the flavonoid quercetin reduces obesity-induced hepatic inflammation by inducing HO-1, which promotes hepatic macrophage polarization in favor of the M2 phenotype. MATERIALS/METHODS: Male C57BL/6 mice were fed a regular diet (RD), high-fat diet (HFD), or HFD supplemented with quercetin (HF+Que, 0.5g/kg diet) for nine weeks. Inflammatory cytokines and macrophage markers were measured by ELISA and RT-PCR, respectively. HO-1 protein was measured by Western blotting. RESULTS: Quercetin supplementation decreased levels of inflammatory cytokines ($TNF{\alpha}$, IL-6) and increased that of the anti-inflammatory cytokine (IL-10) in the livers of HFD-fed mice. This was accompanied by upregulation of M2 macrophage marker genes (Arg-1, Mrc1) and downregulation of M1 macrophage marker genes ($TNF{\alpha}$, NOS2). In co-cultures of lipid-laden hepatocytes and macrophages, treatment with quercetin induced HO-1 in the macrophages, markedly suppressed expression of M1 macrophage marker genes, and reduced release of MCP-1. Moreover, these effects of quercetin were blunted by an HO-1 inhibitor and deficiency of nuclear factor E2-related factor 2 (Nrf2) in macrophages. CONCLUSIONS: Quercetin reduces obesity-induced hepatic inflammation by promoting macrophage phenotype switching. The beneficial effect of quercetin is associated with Nrf2-mediated HO-1 induction. Quercetin may be a useful dietary factor for protecting against obesity-induced steatohepatitis.

• The Korean Journal of Physiology and Pharmacology
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• 제15권2호
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• pp.101-106
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• 2011

We demonstrate that glycoprotein isolated from Dioscorea batatas (GDB) has immunostimulatory effects including macrophage activation. Analysis of infiltration of inflammatory cells into peritoneal cavity showed GDB treatment significantly increased the recruitment of macrophages, lymphocytes, neutrophils, and monocytes into the peritoneal cavity. Treatment of spleen cells isolated from C57BL/6 mice with GDB significantly increased the proliferation of B cells and T cells induced by LPS and ConA, respectively. Treatment with GDB significantly increased the cytolytic capacity of NK cells and macrophages against YAC-1 and B16 cells, respectively. In order to further confirm and investigate the mechanism of GDB on macrophage activation, we analyzed the effects of GDB on the cytokine expression including iNOS, IL-1${\beta}$, and TNF-${\alpha}$ in mouse macrophage cell line, RAW 264.7 cells. RT-PCR and ELISA showed that GDB increased the expression of IL-1${\beta}$, and TNF-${\alpha}$, whereas iNOS was not induced by GDB. Collectively, this series of experiments indicates that GDB stimulates immune system including macrophage activation.

• 대한한방내과학회지
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• 제31권2호
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• pp.346-355
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• 2010

Objectives : This study was performed in order to investigate the anti-fibrogenic effect of Acer tegmentosum Maxim. on r at hepatic stellate cell line T6. Materials and Methods : Hepatic stellate Cells (T6) were treated with various concentrations of distilled water Acer teg mentosum Maxim. extract for 24, 48, 72 hours. After the treatment, cell viability, proliferation, procollagen levels, mRNA of AS MA, MMP-2, collagen type 1a2 and IL-6 production were measured using MTT assay, BrdU assay, RT-PCR, procollagen typ e 1 C-peptide EIA kit and murine IL-6 ELISA development kit. Results : Cell viability of HSC-T6 decreased significantly in both 24 hours and 48 hours groups in a dose-dependant man ner. Proliferation of HSC also decreased in the same way. In the RT-PCR, mRNA expression of collagen type 1a2 and ASMA decreased in the groups which were treated with Acer tegmentosum Maxim. for 24 hours. The production of procollagen tended to decrease in a dose-dependant manner in the 24 hours treated group. IL-6 production increased under Acer tegmentosum trea tment in a dose-dependant manner in both 24 and 48 hours groups. Conclusion : These results show the possibility that Acer tegmentosum Maxim. can be an effective remedy for liver fibrosi s and liver cirrhosis.

• 동의생리병리학회지
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• 제28권1호
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• pp.45-52
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• 2014

Hoesaeng-san is known to be effective for treating diarrhea and vomiting. However the therapeutic mechanism of Hoesaeng-san is still not well understood. The aim of the present study was to demonstrate the effects of Hoesaeng-san ethanol extract (HSSEE) on the expression of pro-inflammatory cytokines, as well as to elucidate its mechanism of action in the human mast cell line (HMC-1). Mast Cell were stimulated with phorbol 12-myristate 13-acetate (PMA) plus A23187 in the presence or absence of HSSEE. To study the possible effects of HSSEE, ELISA, RT-PCR, Western blot analysis were used in this study. HSSEE significantly inhibited the PMA plus A23187-induction of inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-8. In activated HMC-1 cells, phosphorylation of extra-signal response kinase (ERK) 1/2 and c-jun n-terminal kinase (JNK)1/2 decreased after treatment with HSSEE. Moreover HSSEE inhibited PMA plus A23187-induced nuclear factor (NF)-${\kappa}B$ activation and $I{\kappa}B$ degradation. HSSEE suppressed the expression of TNF-${\alpha}$, IL-6, IL-8 through a decrease in the ERK 1/2 and JNK 1/2, as well as activation of NF-${\kappa}B$. These results indicated that HSSEE exerted a regulatory effect on inflammatory reactions mediated by mast cells.