• 한국응용과학기술학회지
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• 제33권1호
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• pp.13-22
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• 2016

밀싹 추출물의 생리활성 및 화장품 소재로서의 가능성 여부를 규명하고자 하였다. 본 연구는 세포실험을 통해 밀싹 추출물의 피부 세포에 대한 독성을 확인하고, 피부 세포 미백 활성 및 노화에 대한 연구를 수행하여 기능성 화장품 소재로서의 가능성을 알아보고자 하였다. 본 연구 결과 밀싹 추출물이 HDF, B16F10 세포에 대한 독성이 적은 것으로 확인되었다. 멜라닌 생합성 억제에 대한 효과는 약한 것으로 확인되었으나, 자외선에 유도되는 MMP-1의 발현을 저해함으로써 피부의 광노화를 억제하는 효과를 통해 광노화에 의한 피부 주름과 자연 노화에 의한 피부 주름을 예방하는데 유의한 효과를 가질 수 있음을 확인하였다. 따라서 본 연구는 밀싹 추출물의 기능성 화장품 소재로 사용 시 피부 노화 예방 관점에서의 기능성 화장품 소재로 매우 유용하게 활용될 수 있을 것으로 사료된다.

• Restorative Dentistry and Endodontics
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• 제38권4호
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• pp.204-209
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• 2013

Objectives: The objective of this in vitro study was to evaluate and compare the cytotoxicity of four different root canal sealers i.e. Apexit Plus (Ivoclar Vivadent), Endomethasone N (Septodont), AH-26 (Dentsply) and Pulpdent Root Canal Sealer (Pulpdent), on a mouse fibroblast cell line (L929). Materials and Methods: Thirty two discs for each sealer (5 mm in diameter and 2 mm in height) were fabricated in Teflon mould. The sealer extraction was made in cell culture medium (Dulbecco's Modified Eagle's Medium, DMEM) using the ratio 1.25 $cm^2/mL$ between the surface of the sealer samples and the volume of medium in a shaker incubator. Extraction of each sealer was obtained at 24 hr, 7th day, 14th day, and one month of interval. These extracts were incubated with L929 cell line and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) assay was done. Two-way ANOVA for interaction effects between sealer and time and Post-hoc multiple comparison using Tukey's test across all the 16 different groups were used for statistical analysis. Results: Apexit Plus root canal sealer was significantly less toxic than other sealers (p < 0.05) and showed higher cellular growth than control. Endomethasone N showed mild cytotoxicity. AH-26 showed severe toxicity which became mild after one month while Pulpdent Root Canal Sealer showed severe to moderate toxicity. Conclusions: Apexit Plus was relatively biocompatible sealer as compared to other three sealers which were cytotoxic at their initial stages, however, they became biocompatible with time.

• 한방재활의학과학회지
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• 제20권2호
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• pp.51-61
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• 2010

Objectives : The purpose of this study was to investigate antioxidant effects of curcumin from Curcumae Longae Radix. Methods : Using HepG2 Iiver-like cells, the antioxidant effects of curcumin, one of main components from Curcumae Longae Radix, and its analogues have been evaluated by measuring their effects on cytotoxicity induced by $H_2O_2$. Results : The pre-incubation for 6 hours with curcumin, bis-demethoxycurcumin, or dimethoxycurcumin protected HepG2 cells from $H_2O_2$-induced toxicity in a dose-dependent manner. However, tetrahydrocurcumin, one of curcumin metabolites, did not protect HepG2 cells from $H_2O_2$-induced toxicity. Interestingly, curcumin, bis-demethoxycurcumin, and dimethoxycurcumin were increased in the protein levels of heme oxygenase-1(HO-1) at concentrations that were also effective in cellular protection. In contrast, tetrahydrocurcumin did not induce HO-1 expression. Tin protoporphyrin-IX, an inhibitor of HO-1 activity, significantly abolished cytoprotection afforded by curcumin, bis-demethoxycurcumin and dimethoxycurcumin. Conclusions : These results demonstrate that curcumin, bis-demethoxycurcumin, and dimethoxycurcumin with two conjugated doble bonds on their structures may reduce $H_2O_2$-induced oxidative stress through HO-1 expression. HO-1 induction may be one of antioxidant pathways by which curcumin protects from oxidative stress-induced cytotoxicity.

• Molecular & Cellular Toxicology
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• 제2권1호
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• pp.35-47
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• 2006

2, 3, 7, 8-Tetrachlorodibenzo-p-dioxin (TCDD) are well known as the most toxic environmental compound in these days. Many researches are reported that dioxin produces multiple toxic effects, such as endocrine toxicity, reproductive toxicity, immunotoxicity and cancer. In this study, we carried to discover novel evidence for previously unknown gene expression patterns in human exposed to dioxin by using radioactive cDNA microarray. 548 workers who were divided into experimental and control groups according to their urinary Naphthol levels were enrolled in our study. Blood mRNA in human was isolated, and the gene expression profiles were analyzed by cDNA microarray. Gene expression analysis identified 52 genes which exhibited a significant change. In our study, most notably, genes involved in cell cycle, cell proliferation, signal transduction and apoptosis in human exposed to dioxin, such as CCND3, TSHR, and EFRN5, were up-regulated. In the current study, we observed gene expression of people that are exposed to dioxin using radioactive cDNA microarray. Through these results, we suggest when objects are exposed to toxic compounds, such as dioxin, the radioactive cDNA microarray may be using in sensitively detecting of cancerous change.

• 통합자연과학논문집
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• 제7권1호
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• pp.25-38
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• 2014

Amyloid-${\beta}$-peptide ($A{\beta}$) is important in the pathogenesis of Alzheimer's disease (AD). Calpain ($Ca^{2+}$-dependent protease) and caspase-8 (the initiating caspase for the extrinsic, receptor-mediated apoptosis pathway) have been implicated in $AD/A{\beta}$ toxicity. We found that $A{\beta}$ promoted degradation of calpastatin (the specific endogenous calpain inhibitor); calpastatin degradation was prevented by inhibitors of either calpain or caspase-8. The results implied a cross-talk between the two proteases and suggested that one protease was responsible for the activity of the other one. In neuron-like differentiated PC12 cells, calpain promotes active caspase-8 formation from procaspase-8 via the $A{\beta}$ and CD95 pathways, along with degradation of the procaspase-8 processing inhibitor caspase-8 (FLICE)-like inhibitory protein, short isoform (FLIPS). Inhibition of calpain (by pharmacological inhibitors and by overexpression of calpastatin) prevents the cleavage of procaspase-8 to mature, active caspase-8, and inhibits FLIPS degradation in the $A{\beta}$-treated and CD95-triggered cells. Increased cellular Ca2+ per se results in calpain activation but does not lead to caspase-8 activation or FLIPS degradation. The results suggest that procaspase-8 and FLIPS association with cell membrane receptor complexes is required for calpain-induced caspase-8 activation. The results presented here add to the understanding of the roles of calpain, caspase- 8, and CD95 pathway in $AD/A{\beta}$ toxicity. Calpain-promoted activation of caspase-8 may have implications for other types of CD95-induced cell damage, and for nonapoptotic functions of caspase-8. Inhibition of calpain may be useful for modulating certain caspase-8-dependent processes.

• Genes and Genomics
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• 제40권11호
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• pp.1199-1211
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• 2018

Soil acidification is one of major problems limiting crop growth and especially becoming increasingly serious in China owing to excessive use of nitrogen fertilizer. Only the STOP1 of Arabidopsis was identified clearly sensitive to proton rhizotoxicity and the molecular mechanism for proton toxicity tolerance of plants is still poorly understood. The main objective of this study was to investigate the transcriptomic change in plants under the low pH stress. The low pH as a single factor was employed to induce the response of the wheat seedling roots. Wheat cDNA microarray was used to identify differentially expressed genes (DEGs). A total of 1057 DEGs were identified, of which 761 genes were up-regulated and 296 were down-regulated. The greater percentage of up-regulated genes involved in developmental processes, immune system processes, multi-organism processes, positive regulation of biological processes and metabolic processes of the biological processes. The more proportion of down-regulation genes belong to the molecular function category including transporter activity, antioxidant activity and molecular transducer activity and to the extracellular region of the cellular components category. Moreover, most genes among 41 genes involved in ion binding, 17 WAKY transcription factor genes and 17 genes related to transport activity were up-regulated. KEGG analysis showed that the jasmonate signal transduction and flavonoid biosynthesis might play important roles in response to the low pH stress in wheat seedling roots. Based on the data, it is can be deduced that WRKY transcription factors might play a critical role in the transcriptional regulation, and the alkalifying of the rhizosphere might be the earliest response process to low pH stress in wheat seedling roots. These results provide a basis to reveal the molecular mechanism of proton toxicity tolerance in plants.

• Journal of Ginseng Research
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• 제46권4호
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• pp.572-584
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• 2022

Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests, survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK and reduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density and lifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2 protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedly enhanced lifespan in the transgenic mouse model (R6/2) of HD.

• 대한본초학회지
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• 제28권5호
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• pp.61-68
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• 2013

Objectives : Hibisci Flos has long been used for inflammatory diseases in traditional Korean medicine. However, little scientific investigation has been carried out. The aim of the present study is to investigate the effect of Hibisci Flos water extract (HF) on inflammatory cytokines production in Raw 264.7 cells stimulated by lipopolysaccaride (LPS). Method : HF was prepared by extracting with boiling water for 2 hours. We observed the cell viability of mouse macrophage Raw 264.7, the production of nitric oxide (NO) and the inflammatory cytokines such as interleukin (IL)-4, IL-5, IL-10, IL-15, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interferon-gamma (IFN-${\gamma}$), vascular endothelial growth factor (VEGF), granulocyte macrophage-colony stimulating factor (GM-CSF), and macrophage colony-stimulating factor (M-CSF) in Raw 264.7 cells stimulated by LPS. Result : The MTT assay was carried out to check the cellular toxicity of HF. No significant toxicity was observed in the experiment. HF significantly inhibited the increase of NO in the macrophages induced by LPS after 24 hour treatment. HF significantly inhibited the production of IL-4, IL-5, IL-10, IL-15, TNF-${\alpha}$, IFN-${\gamma}$, VEGF, GM-CSF and M-CSF in the Raw 264.7 cells induced by LPS in the concentration of $25{\mu}g/mL$ or higher. Conclusion : These results suggest that HF might have regulatory effects on LPS-induced inflammatory cytokine production, which might explain its beneficial effect in the treatment of inflammatory disease.

• 대한수의학회지
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• 제63권3호
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• pp.30.1-30.8
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• 2023

Metformin is a treatment used widely for non-insulin-dependent diabetes mellitus with few side effects and acts by inhibiting hepatic gluconeogenesis and glucose absorption from the gastrointestinal tract. Lymphoma is one of the most common hematological malignancies in dogs. Chemotherapy is used mainly on lymphoma, but further research on developing anticancer drugs for lymphoma is needed because of its severe side effects. This study examined the anticancer effects of metformin alone and in combination with 2-deoxy-D-glucose (2-DG), a glucose analog, on EL4 cells (mouse T cell lymphoma). Metformin reduced the metabolic activity of EL4 cells and showed an additive effect when combined with 2-DG. In addition, cell death was confirmed using a trypan blue exclusion test, Hochest 33342/propidium iodide (PI) staining, and Annexin V/PI staining. An analysis of the cell cycle and mitochondria membrane potential (MMP) to investigate the mechanism of action showed that metformin stopped the G2/M phase of EL4 cells, and metformin + 2-DG decreased MMP. Metformin exhibited anticancer effects as a G2/M phase arrest mechanism in EL4 cells and showed additive effects when combined with 2-DG via MMP reduction. Unlike cytotoxic chemotherapeutic anticancer drugs, metformin and 2-DG are related to cellular glucose metabolism and have little toxicity. Therefore, metformin and 2-DG can be an alternative to reduce the toxicity caused by chemotherapeutic anticancer drugs. Nevertheless, research is needed to verify the in vivo efficacy of metformin and 2-DG before they can be used in lymphoma treatments.

• Molecules and Cells
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• 제47권1호
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• pp.100005.1-100005.15
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• 2024

Amyotrophic lateral sclerosis is a devastating neurodegenerative disease with a complex genetic basis, presenting both in familial and sporadic forms. The hexanucleotide (G₄C₂) repeat expansion in the C9orf72 gene, which triggers distinct pathogenic mechanisms, has been identified as a major contributor to familial and sporadic Amyotrophic lateral sclerosis cases. Animal models have proven pivotal in understanding these mechanisms; however, discrepancies between models due to variable transgene sequence, expression levels, and toxicity profiles complicate the translation of findings. Herein, we provide a systematic comparison of 7 publicly available Drosophila transgenes modeling the G₄C₂ expansion under uniform conditions, evaluating variations in their toxicity profiles. Further, we tested 3 previously characterized disease-modifying drugs in selected lines to uncover discrepancies among the tested strains. Our study not only deepens our understanding of the C9orf72 G₄C₂ mutations but also presents a framework for comparing constructs with minute structural differences. This work may be used to inform experimental designs to better model disease mechanisms and help guide the development of targeted interventions for neurodegenerative diseases, thus bridging the gap between model-based research and therapeutic application.