• Journal of Microbiology and Biotechnology
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• 제26권2호
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• pp.277-286
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• 2016

Makgeolli lees (ML) has several physiological effects such as antioxidant, antidiabetic, and anticancer properties, but its biological functions have not been determined definitively. Here, we tested whether ML has a cytoprotective effect on paraquat (PQ)-induced oxidative stress in the human lung carcinoma cell line A549. At 0.1 mg/ml ML, viability of PQ-exposed A549 cells was restored by 12.4%, 18.5%, and 48.6% after 24, 48, and 72 h, respectively. ML also reduced production of the intracellular reactive oxygen species (ROS) that were generated by PQ treatment. Further experiments revealed that ML treatment enhanced the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) as well as ARE-GFP reporter activity. ML treatment also effectively increased the expression of NRF2's target genes NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase 1 (HO-1). Moreover, we found that expression of cytoprotective genes, including glutathione peroxidases (GPXs), superoxide dismutase (SOD1), catalase (CAT), peroxiredoxin 3 (PRDX3), and peroxiredoxin 4 (PRDX4), was greatly enhanced by treatment with ML during PQ exposure. Taken together, the data suggest that treatment of PQ-exposed A549 cells with ML ameliorates cytotoxicity through induction of NRF2 expression and its target genes HO-1, NQO1, and other antioxidant genes. Thus, ML may serve as a functional food applicable to ROS-mediated human diseases.

• Journal of Ginseng Research
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• 제44권1호
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• pp.50-57
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• 2020

Background: The cellular senescence of primary cultured cells is an irreversible process characterized by growth arrest. Restoration of senescence by ginsenosides has not been explored so far. Rg3(S) treatment markedly decreased senescence-associated β-galactosidase activity and intracellular reactive oxygen species levels in senescent human dermal fibroblasts (HDFs). However, the underlying mechanism of this effect of Rg3(S) on the senescent HDFs remains unknown. Methods: We performed a label-free quantitative proteomics to identify the altered proteins in Rg3(S)-treated senescent HDFs. Upregulated proteins induced by Rg3(S) were validated by real-time polymerase chain reaction and immunoblot analyses. Results: Finally, 157 human proteins were identified, and variable peroxiredoxin (PRDX) isotypes were highly implicated by network analyses. Among them, the mitochondrial PRDX3 was transcriptionally and translationally increased in response to Rg3(S) treatment in senescent HDFs in a time-dependent manner. Conclusion: Our proteomic approach provides insights into the partial reversing effect of Rg3 on senescent HDFs through induction of antioxidant enzymes, particularly PRDX3.

• Journal of Microbiology and Biotechnology
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• 제25권8호
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• pp.1380-1389
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• 2015

Prx1, an AhpF-dependent 2-Cys peroxiredoxin (Prx), was previously identified in Vibrio vulnificus, a facultative aerobic pathogen. In the present study, transcription of the V. vulnificus prx1ahpF genes, which are adjacently located on the chromosome, was evaluated by analyzing the promoter and intergenic region of the two genes. Northern blot analyses revealed that transcription of prx1ahpF results in two transcripts, the prx1 and prx1ahpF transcripts. Primer extension analysis and a point mutational analysis of the promoter region showed that the two transcripts are generated from a single promoter. In addition, the 3' end of the prx1 transcript at the prx1ahpF intergenic region was determined by a 3'RACE assay. These results suggested that the prx1ahpF genes are transcribed as an operon, and the prx1 transcript was produced by transcriptional termination in the intergenic region. RNA secondary structure prediction of the prx1ahpF intergenic region singled out a stem-loop structure without poly(U) tract, and a deletion analysis of the intergenic region showed that the atypical stem-loop structure acts as the transcriptional attenuator to result in the prx1 and prx1ahpF transcripts. The combined results demonstrate that the differential expression of prx1 and ahpF is accomplished by the cis-acting transcriptional attenuator located between the two genes and thereby leads to the production of a high level of Prx1 and a low level of AhpF.

• The Korean Journal of Physiology and Pharmacology
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• 제16권6호
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• pp.463-468
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• 2012

Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic ${\beta}$-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic ${\beta}$-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic ${\beta}$-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic ${\beta}$-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic ${\beta}$ cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.

• Molecules and Cells
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• 제39권1호
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• pp.65-71
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• 2016

A challenge in the redox field is the elucidation of the molecular mechanisms, by which $H_2O_2$ mediates signal transduction in cells. This is relevant since redox pathways are disturbed in some pathologies. The transcription factor OxyR is the $H_2O_2$ sensor in bacteria, whereas Cys-based peroxidases are involved in the perception of this oxidant in eukaryotic cells. Three possible mechanisms may be involved in $H_2O_2$ signaling that are not mutually exclusive. In the simplest pathway, $H_2O_2$ signals through direct oxidation of the signaling protein, such as a phosphatase or a transcription factor. Although signaling proteins are frequently observed in the oxidized state in biological systems, in most cases their direct oxidation by $H_2O_2$ is too slow ($10^1M^{-1}s^{-1}$ range) to outcompete Cys-based peroxidases and glutathione. In some particular cellular compartments (such as vicinity of NADPH oxidases), it is possible that a signaling protein faces extremely high $H_2O_2$ concentrations, making the direct oxidation feasible. Alternatively, high $H_2O_2$ levels can hyperoxidize peroxiredoxins leading to local building up of $H_2O_2$ that then could oxidize a signaling protein (floodgate hypothesis). In a second model, $H_2O_2$ oxidizes Cys-based peroxidases that then through thiol-disulfide reshuffling would transmit the oxidized equivalents to the signaling protein. The third model of signaling is centered on the reducing substrate of Cys-based peroxidases that in most cases is thioredoxin. Is this model, peroxiredoxins would signal by modulating the thioredoxin redox status. More kinetic data is required to allow the identification of the complex network of thiol switches.

• Tuberculosis and Respiratory Diseases
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• 제59권2호
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• pp.142-150
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• 2005

연구배경 : Peroxiredoxin (Prx) 은 최근에 알려진 항산화제로 세포의 증식과 분화, 세포사멸이나 발암과정에 관여하는 것으로 알려져 있다. 하지만, 현재까지 폐암을 비롯한 각종 질병에서의 이들 Prx단백의 역할은 잘 규명되어 있지 않다. 이에 본 연구는 폐암 조직과 정상폐조직에서 Prx 단백의 발현 양상과 분포를 연구하여 이들의 병태 생리학적인 의미를 찾아보고자 하였다. 방 법 : 아주대학교 병원에서 폐암으로 진단된 환자의 폐암조직과, 동일 환자의 정상 폐조직에서, 1 차원전기영동 (reducing 조건과 non-reducing 조건에서의 SDSPAGE) 혹은 2차원전기영동을 시행한 후 Western blot으로 Prx, Trx 및 TR의 발현 양상을 분석 하였으며, 백서의 정상 폐조직과, 환자의 폐암 조직에서 anti-Prx rabbit polyclonal 항체로 하여 면역조직화학염색법을 통해, Prx 단백의 분포를 관찰하였다. 결 과 : 면역조직화학염색법 결과 백서의 정상 폐조직에서는 Prx I, II, III 및 V 유형이, 주로 기관지상피세포, 폐포상피세포 및 폐포대식세포에서 발현되고 있음을 관찰하였다. 인체 폐암조직에서는, 정상 폐조직 부위에 비해서 Prx I 과 Prx III 유형 및 Trx단백의 발현이 선택적으로 증가되어 있고, 특히, 2차원 전기영동을 통한 프로티옴 분석에서 산화된 형태의 Prx I 과 Prx II가 증가 한 것을 비롯하여, 분자량과 등전점(pI)이 약간 변화된 형태의 Prx III가 폐암조직에 존재함을 알 수 있었다. 한편, 폐암 조직의 non-reducing 전기영동 후 Western blot에서는, monomer와 dimer 사이의 중간 크기에 해당하는 약 40 kDa과 200 kDa 이상 크기의, 항 Prx 항체와 반응하는 단백 띠 (reactive bands)가 관찰되었다. 결 론 : 폐암 조직에서 관찰되는 Prx I 과 Prx III 유형 및 Trx의 과발현 양상은, 종양 세포들이 주변의 미세 환경으로부터 겪는 여러 스트레스에 대하여 단백질을 보호하고 세포의 생명력을 유지하는데 있어 주요한 역할을 하는 것으로 사료된다.

• BMB Reports
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• 제44권8호
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• pp.497-505
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• 2011

Reactive oxygen species (ROS), which include superoxide anions and peroxides, induce oxidative stress, contributing to the initiation and progression of cardiovascular diseases involving atherosclerosis. The endogenous and exogenous factors hypercholesterolemia, hyperglycemia, hypertension, and shear stress induce various enzyme systems such as nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, and lipoxygenase in vascular and immune cells, which generate ROS. Besides inducing oxidative stress, ROS mediate signaling pathways involved in monocyte adhesion and infiltration, platelet activation, and smooth muscle cell migration. A number of antioxidant enzymes (e.g., superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins) regulate ROS in vascular and immune cells. Atherosclerosis results from a local imbalance between ROS production and these antioxidant enzymes. In this review, we will discuss 1) oxidative stress and atherosclerosis, 2) ROS-dependent atherogenic signaling in endothelial cells, macrophages, and vascular smooth muscle cells, 3) roles of peroxidases in atherosclerosis, and 4) antioxidant drugs and therapeutic perspectives.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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• pp.67-67
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• 2002

The imbalance between reactive oxygen species(ROS) production and total antioxidant capacity reproduction system is correlated with infertility. Therefore, this study was designed to investigate the expression patterns of peroxiredoxin(Prx), a member of antioxidant family, in reproductive system that includes testis, epididymis ovary, oviduct, and uterus. (omitted)

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVII)
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• pp.682-682
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• 2005

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVII)
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• pp.686-686
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• 2005