• 한국식품영양과학회지
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• 제44권7호
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• pp.1079-1083
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• 2015

본 연구는 양조과정의 부산물인 주박으로부터 분리한 다당류(JPS)가 초기 면역반응에 중추적인 역할을 수행하는 대식세포에서 활성화를 유도하는지에 관한 여부를 알아보기 위해서 수행되었다. 주박에서 분리한 다당류를 마우스 유래 대식세포인 RAW264.7 cell에 처리하였을 때 대식세포의 활성화의 지표인 NO와 cytokine(IL-6, TNF-${\alpha}$)의 분비가 증가되었다. 또한 이러한 NO와 cytokine의 증가의 원인에 관한 면역기전에 관하여 알아본 결과 JPS의 처리는 MAPKs(ERK, JNK, p-38)의 인산화를 촉진시켜 NF-${\kappa}B$의 활성을 유도하여 면역세포의 활성인자들의 분비를 촉진시킨 것으로 관찰되었다.

• Journal of Periodontal and Implant Science
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• 제43권4호
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• pp.191-197
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• 2013

Purpose: Nitric oxide (NO) is a short-lived bioactive molecule that is known to play an important role in the pathogenesis of periodontal disease. In the current study, we investigated the effect of the flavonoid quercetin on the production of NO in murine macrophages activated with lipopolysaccharide (LPS) from Prevotella intermedia, a pathogen related to inflammatory periodontal disease, and tried to elucidate the underlying mechanisms of action. Methods: LPS was isolated from P. intermedia ATCC 25611 cells by the standard hot phenol-water method. The concentration of NO in cell culture supernatants was determined by measuring the accumulation of nitrite. Inducible NO synthase (iNOS) and heme oxygenase-1 (HO-1) protein expression, phosphorylation of c-Jun N-terminal kinase (JNK) and p38, inhibitory ${\kappa}B$ $(I{\kappa}B)-{\alpha}$ degradation, and signal transducer and activator of transcription 1 (STAT1) phosphorylation were analyzed via immunoblotting. Results: Quercetin significantly attenuated iNOS-derived NO production in RAW246.7 cells activated by P. intermedia LPS. In addition, quercetin induced HO-1 protein expression in cells activated with P. intermedia LPS. Tin protoporphyrin IX (SnPP), a competitive inhibitor of HO-1, abolished the inhibitory effect of quercetin on LPS-induced NO production. Quercetin did not affect the phosphorylation of JNK and p38 induced by P. intermedia LPS. The degradation of $I{\kappa}B-{\alpha}$ induced by P. intermedia LPS was inhibited when the cells were treated with quercetin. Quercetin also inhibited LPS-induced STAT1 signaling. Conclusions: Quercetin significantly inhibits iNOS-derived NO production in murine macrophages activated by P. intermedia LPS via anti-inflammatory HO-1 induction and inhibition of the nuclear factor-${\kappa}B$ and STAT1 signaling pathways. Our study suggests that quercetin may contribute to the modulation of host-destructive responses mediated by NO and appears to have potential as a novel therapeutic agent for treating inflammatory periodontal disease.

• Molecules and Cells
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• 제44권7호
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• pp.458-467
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• 2021

GPR43 (also known as FFAR2 or FFA2) is a G-protein-coupled receptor primarily expressed in immune cells, enteroendocrine cells and adipocytes that recognizes short-chain fatty acids, such as acetate, propionate, and butyrate, likely to be implicated in innate immunity and host energy homeostasis. Activated GPR43 suppresses the cAMP level and induces Ca²⁺ flux via coupling to Gα_i and Gα_q families, respectively. Additionally, GPR43 is reported to facilitate phosphorylation of ERK through G-protein-dependent pathways and interacts with β-arrestin 2 to inhibit NF-κB signaling. However, other G-protein-dependent and independent signaling pathways involving GPR43 remain to be established. Here, we have demonstrated that GPR43 augments Rho GTPase signaling. Acetate and a synthetic agonist effectively activated RhoA and stabilized YAP/TAZ transcriptional coactivators through interactions of GPR43 with Gα_q/11 and Gα_12/13. Acetate-induced nuclear accumulation of YAP was blocked by a GPR43-specific inverse agonist. The target genes induced by YAP/TAZ were further regulated by GPR43. Moreover, in THP-1-derived M1-like macrophage cells, the Rho-YAP/TAZ pathway was activated by acetate and a synthetic agonist. Our collective findings suggest that GPR43 acts as a mediator of the Rho-YAP/TAZ pathway.

• 대한정형외과학회지
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• 제54권6호
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• pp.478-489
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• 2019

골관절염은 관절연골 침식의 진행을 특징적으로 보이는 질환으로 관절운동 중에 통증을 증가시키고 기계적 스트레스를 견디는 능력을 감소시켜 결과적으로 관절의 가동성과 기능을 저하시킨다. 외상 또는 퇴행성으로 인한 관절연골의 손상이 일반적 관절염의 주요 원인으로 생각되며 이러한 관절연골 손상의 재생에 관한 수많은 연구와 시도들이 현재까지 진행되어 오고 있다. 현재까지 연골 손상의 경우 미세골절술과 자가연골세포 이식술이 일반적인 수술적 치료방법으로 제시되어 왔으나 비교적 양호한 임상 결과에도 불구하고 정상 유리연골의 생성이 미흡하여 시간이 경과하면서 결과가 악화되는 등 단점이 있다. 이를 보완하기 위하여 줄기세포 기반 치료법이 개발되었다. 이 종설에서는 현재 사용되는 다양한 연골 재생 방법들의 장단점 및 결과에 대해 요약하고 특히 중간엽 줄기세포(mesenchymal stem cells) 기반 연골 재생 치료법을 논하고 나아가 이상적인 미래 연골 재생 치료법에 대해서도 고민해보고자 한다.

• Journal of Veterinary Science
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• 제24권5호
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• pp.55.1-55.12
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• 2023

Background: Peste des petits ruminants (PPR), caused by the PPR virus (PPRV), is an acute and fatal contagious disease that mainly infects goats, sheep, and other artiodactyls. Peripheral blood mononuclear cells (PBMCs) are considered the primary innate immune cells. Objectives: PBMCs derived from goats were infected with PPRV and analyzed to detect the relationship between PPRV replication and apoptosis or the inflammatory response. Methods: Quantitative real-time polymerase chain reaction was used to identify PPRV replication and cytokines expression. Flow cytometry was conducted to detect apoptosis and the differentiation of CD4⁺ and CD8⁺ T cells after PPRV infection. Results: PPRV stimulated the differentiation of CD4⁺ and CD8⁺ T cells. In addition, PPRV induced apoptosis in goat PBMCs. Furthermore, apoptosis and the inflammatory response induced by PPRV could be suppressed by Z-VAD-FMK and Z-YVAD-FMK, respectively. Moreover, the virus titer of PPRV was attenuated by inhibiting caspase-1-dependent apoptosis and inflammation. Conclusions: This study showed that apoptosis and the inflammatory response play an essential role in PPR viral replication in vitro, providing a new mechanism related to the cell host response.

• Molecules and Cells
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• 제24권3호
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• pp.372-377
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• 2007

The orphan nuclear receptor, SF-1, plays a pivotal role in the development and differentiation of the endocrine and reproductive systems, and also regulates the transcription of a host of genes, including those encoding several steroidogenic enzymes and gonadotropins. We found that a previously unidentified repressor, EID-1, is an SF-1-interacting protein that inhibits the transactivation of SF-1. A transient transfection assay revealed that EID-1 inhibits SF-1, but not LRH-1, $ERR{\gamma}$, or mCAR. Using the yeast two hybrid and GST pull-down assays, we determined that EID-1 interacted strongly with SF-1. In addition, it colocalized with SF-1 in mammalian cells and interacted specifically with the AF-2 domain of SF-1, competing with SRC-1 to inhibit SF-1 transactivation. EID-1 is expressed in the mouse testis, and its expression decreases during testis development. The results of the present study suggest that EID-1 can act as a repressor, regulating the function of SF-1.

• Parasites, Hosts and Diseases
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• 제38권4호
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• pp.209-236
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• 2000

The last two decades witnessed significant advances in the efforts of immune-parasitologists to elucidate the nature and role of the host mucosal defence mechanisms against intestinal nematode parasites. Aided by recent advances in basic immunology and biotechnology with the concomitant development of well defined laboratory models of infection, immunoparasitologists have more precisely analyzed and defined the different immune effector mechanisms during the infection; resulting in great improvement in our current knowledge and understanding of protective immunity against gastrointestinal (GI) nematode parasites. Much of this current understanding comes from experimental studies in laboratory rodents, which have been used as models of livestock and human GI nematode infections. These rodent studies, which have concentrated on Heligmosomoides polygyrus, Nippostrongylus brasiliensis, Strongyloides ratti/5. venezuelensis. Trichinella spiralis and trichuris muris infections in mice and rats, have helped in defining the types of T cell responses that regulate effector mechanisms and the effector mechanisms responsible for worm expulsion. In addition, these studies bear indications that traditionally accepted mechanisms of resistance such as eosinophilia and IgE responses may not play as important roles in protection as were previously conceived. In this review, we shall, from these rodent studies, attempt an overview of the mucosal and other effector responses against intestinal nematode parasites beginning with the indices of immune protection as a model of the protective immune responses that may occur in animals and man.

• 한국미생물·생명공학회지
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• 제24권4호
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• pp.408-414
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• 1996

The SecY is a central component of the protein export machinery that mediate the translocation of secretory proteins across the plasma membrane, and has been known to be rate-limiting factor of secretion in Escherichia coli. In order to study the extracellular protein secretion in Gram-positive microorganism, we have, constructed strains harboring more than one copy of the gene for SecY. Firstly, the gene, for B. subtilis SecY and its promoter region was subcloned into pDH32 and the chimeric vector was inserted into amyE locus by homologous recombination. Secondly, low copy number vector, pCED6, was also used for subcloning the secY gene and for constructing a strain which harbors several copies of secY. The KH1 cell which harbor two copies of secY on the chromosome excreted more extracellular proteins than the wild type PB2. Moreover, the KH2 cells which harbor several copies of secY in pCED6 vector excreted more extracellular proteins than the KH1 cells. Here, we found that the capacity of protein secretion is partly controlled by the number of secY and it is suggested that SecY has also an important role in protein secretion in B. subtilis, a gram positive microorganism, as like in E. coli. This will promote the use of B. subtilis as a host for the expression of useful foreign gene and excretion of precious proteins.

• 한국임상수의학회지
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• 제31권2호
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• pp.156-158
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• 2014

오타리아 물개의 탈모성 피부염에서 Malassezia spp. 를 분리하였다. Sabouraud dextrose agar에서 성장한 집락형태는 유백색에서 황색조로 변연부는 매끄러웠다. 현미경 검경시 형태는 원형에서 실린더형이었고 증식을 지시하는 budding 형이 관찰되었다. 개의 외이염에서 분리한 Malassezia pachydermatis와 비교하기 위해 26s rRNA 염기서열 분석을 실시하여 99.9% 의 일치도를 보였다. Itraconazole pulse therapy는 매우 효과적이었고 재발하지 않았다. 본 증례는 국내 물개에서 발생한 Malassezia 피부염 최초 보고로 판단된다.

• 한국식품영양과학회지
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• 제14권3호
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• pp.305-313
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• 1985

There is a trend that the total number of cancer cases is steadily increasing as the population grows. It has been estimated that 85% of the cancer rate in the U.S. is attributed to environmental factors. Among the environmental factors, diet and nutrition appear to be related to the largest number of human cancers. Diet and nutrition might be related to cancer by several mechanisms. Food may contain a direct carcinogen or precursors that become carcinogens by spontanous reactions, or by host metabolism, or through the actions of microbial flora. Chemicals that cause cancers generally have reactive electrophilic centers which can combine with electron-rich atoms in nucleic acids and cause cancers by changing the genetic activity of the cells. A variety of factors in foods might be involved in the etiology of carcinogenesis. Chemicals in food that cause cancers include carcinogens of plants and animal origin and also those in drinking water. Other then these, fungal metabolites alcohol, asbestos, heavy metals, pesticides, and food additives might be included as food carcinogenesis. The method of cooking foods also might contribute to carcinogenesis. Some chemicals in foods act as promoters in carcinogenesis. Prevention of cancers by dietary practises have received much interest. Consumption of certain vegetables or cellulose can reduce carcinogenic activity of several compounds. A variety of antioxidants or micronutrients may be effective anticarciongens. Glutathione in the soluble fraction of the cells, is a major defense against oxidative and alkylating carcinogens. Recently anticarcinogenic activity of chlorophyll was demonstrated. Daily consumption of milk appears to effectively reduce stomach cancer.