• Molecules and Cells
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• 제39권1호
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• pp.60-64
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• 2016

Inflammation is a pathophysiological response to infection or tissue damage during which high levels of reactive oxygen and nitrogen species are produced by phagocytes to kill microorganisms. Reactive oxygen and nitrogen species serve also in the complex regulation of inflammatory processes. Recently, it has been proposed that peroxiredoxins may play key roles in innate immunity and inflammation. Indeed, peroxiredoxins are evolutionarily conserved peroxidases able to reduce, with high rate constants, hydrogen peroxide, alkyl hydroperoxides and peroxynitrite which are generated during inflammation. In this minireview, we point out different possible roles of peroxiredoxins during inflammatory processes such as cytoprotective enzymes against oxidative stress, modulators of redox signaling, and extracellular pathogen- or damage-associated molecular patterns. A better understanding of peroxiredoxin functions in inflammation could lead to the discovery of new therapeutic targets.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2021년도 춘계학술대회
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• pp.52-52
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• 2021

Persicaria amphibia as an England native plant, is a rhizomatous perennial, one of the rather amphibious plants. Its aquatic form contains water-soluble sugars, starch, and protein. P. amphibia have up to 18% tannins in stems and rhizomes. Previous studies have confirmed the anti-inflammatory activity of live bacteria roots, but no studies on bioactivity are known. DNA damage responses (DDRs) pathways are considered a crucial factor affecting the alleviation of cellular damage. The ataxia-telangiectasia mutated and Rad3 related (ATM) and checkpoint kinase 2 (Chk2) pathways are the main pathways of DNA damage response. Also, p53 is a key integrator of cellular response to oxidative DNA damage, contributing repair, or leading transcription including apoptosis. In the present study, we conducted an investigation into the inhibitory effects of P. amphibia on oxidative DNA damage for confirming potential to complementary medicine and therapies. In conclusion, P. amphibia can provide protective effects against double-stranded DNA break (DSB) caused by oxidative DNA damage.

• Molecular & Cellular Toxicology
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• 제1권2호
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• pp.99-105
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• 2005

Perchloroethylene (tetrachloroethylene, PCE), a dry cleaning and degreasing solvent, can enter ground-water through accidental leak or spills. PCE can be degraded to trichloroethylene (TCE), 1, 1-dichloroethylene (DCE) and vinyl chloride (VC) as potential bio-product. These compounds have been reported that they can cause clinical diseases and cytotoxicity. However, only a little genotoxic information of these compounds has been known. In this study, we investigated DNA single strand breaks of PCE, TCE, DCE and VC by single cell gel electrophoresis assay, (comet assay) which is a sensitive, reliable and rapid method for DNA single strand breaks with mouse lymphoma L5178Y cells. From these results, $37.5\;{\mu}g/ml$ of PCE, $189\;{\mu}g/ml$ of TCE and $56.4\;{\mu}g/ml$ of DCE were revealed significant DNA damages in the absence of S-9 metabolic activation system meaning direct-acting mutagen. And in the presence of S-9 metabolic activation system, $41.5\;{\mu}g/ml$ of PCE, $328.7\;{\mu}g/ml$ of TCE and $949\;{\mu}g/ml$ of DCE were induced significant DNA damage. In the case of VC, it was revealed a significant DNA damage in the presence of S-9 metabolic activation system. Therefore, we suggest that chloroethylene compounds (PCE, TCE, DCE and VC) may be induced the DNA damage in a mammalian cell.

• 한국식품영양학회지
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• 제23권3호
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• pp.306-310
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• 2010

This study was designed to investigate the protective effect of the combination of fucoidan and lutein against AAPH-induced oxidative stress in THP-1 cells. The combination of fucoidan and lutein existed significant antioxidant effect on AAPH-damaged THP-1 cells by using lipid peroxidation and cellular antioxidant capacity assay. Fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) did not affect at all the viability of THP-1 cells, but protected the AAPH-damage of THP-1 cells at the same concentration. The viability of THP-1 cells was 0% with 1 mM AAPH alone, the protective effect of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) was 37% and 36%, respectively. The combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) exhibited significant inhibitory effect of lipid peroxidation using TBARS assay and cellular antioxidant capacity using DCFH-DA assay. In lipid peroxidation, the TBARS value of 1 mM AAPH alone was $0.8{\pm}0.03\;nM$ MDA, its of the combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) was $0.2{\pm}0.05\;nM$ MDA. In cellular antioxidant capacity, the combination of fucoidan($1\;{\mu}g/m{\ell}$) and lutein($10\;{\mu}g/m{\ell}$) exhibited significant cellular antioxidant capacity of 76%, whereas quercetin($10\;{\mu}M$) as positive control exhibited the cellular antioxidant capacity of 32%. These results indicate that the cotreatment of fucoidan and lutein protects against AAPH-induced THP-1 cell damage by inhibiting lipid peroxidation, increasing cellular antioxidant capacity.

• Biomolecules & Therapeutics
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• 제19권3호
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• pp.282-287
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• 2011

Sirt1, a nicotinamide adenine dinucleotide ($NAD^+$)-dependent histone deacetylase, is known to deacetylate a number of proteins that are involved in various cellular pathways such as the stress response, apoptosis and cell growth. Modulation of the stress response by Sirtuin 1 (Sirt1) is achieved by the deacetylation of key proteins in a cellular pathway, and leads to a delay in the onset of cancer or aging. In particular, Sirt1 is known to play an important role in maintaining genomic stability, which may be strongly associated with a protective effect during tumorigenesis and during the onset of aging. In these studies, Sirt1 was generated in stably expressing cells and during the stimulation of DNA damage to examine whether it promotes survival. Sirt1 expressing cells facilitated the repair of DNA damage induced by either ionizing radiation (IR) or bleomycin (BLM) treatment. Fastened damaged DNA repair in Sirt1 expressing cells corresponded to prompt activation of Chk2 and ${\gamma}$-H2AX foci formation and promoted survival. Inhibition of Sirt1 enzymatic activity by a chemical inhibitor, nicotinamide (NIC), delayed DNA damage repair, indicating that promoted DNA damage repair by Sirt1 functions to induce survival when DNA damage occurs.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2023년도 임시총회 및 춘계학술대회
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• pp.54-54
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• 2023

Nypa fruticans Wurmb (N. fruticans) is a plant that belongs to Araceae and N. fruticans is mainly found in tropical mangrove systems. The parts (leaves, stems, and roots) of N. fruticans are traditionally used for asthma, sore throat, and liver disease. N. fruticans contains flavonoids and polyphenols, which are substances that have inhibitory effects on cancer and oxidant. In previous studies, some pharmaceutical effects of N. fruticans on melanogenesis and inflammation have been reported. The present study is conducted to investigate the effect of the ethyl acetate fraction of N. fruticans (ENF) on oxidative DNA damage and UVB-induced DNA damage. DNA damage response (DDR) pathway is important in research on cancer, apoptosis, and so on. DDR pathways are considered a crucial factor affecting the alleviation of cellular damage. ENF could reduce oxidative DNA damage derived from reactive oxygen species by the Fenton reaction. Also, ENF reduced the intensity of intracellular ROS in the live cell image by DCFDA assay. UVB is known to cause skin and cellular damage, then finally contribute to causing the formation of tumors. As for the strategies of reducing DNA damage by UVB, inhibition of p53, H2AX, and Chk2 can be important indexes to protect the human body from DNA damage. As a result of confirming the protective effect of ENF for UVB damage, MMPs significantly decreased, and the expression of apoptosis-related factors tended to decrease. In conclusion, ENF can provide protective effects against double-stranded DNA break (DSB) caused by oxidative DNA damage and UVB-induced DNA damage. These results are considered to be closely related to the protective effect against radicals based on catechin, epicatechin, and isoquercitrin contained in ENF. Based on these results, it is thought that additional mechanism studies for inhibiting cell damage are needed.

• 방사선산업학회지
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• 제7권1호
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• pp.55-59
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• 2013

Ionizing radiation causes the massive generation of reactive oxygen species, resulting in cellular and tissue damage. The present study was performed to evaluate ${\gamma}$-irradiation induced cellular damage in ICR mice. The mice were divided into four groups with ten mice in each group. Group 1 served as an unexposed control group. Groups 2, 3, and 4 were exposed to 3, 5, and 7 Gy of ${\gamma}$-radiation, respectively. Five mice per group were sacrificed 1 and 7 days after ${\gamma}$-radiation. Exposure to ${\gamma}$-irradiation resulted in hematopoietic damage in a dose-dependent manner when compared with the unexposed control group, which featured a significantly decreased spleen index. However, the exposed mice showed no significant differences in their serum AST, ALT and in the histopathological change of their liver. These results suggest that ${\gamma}$-irradiation is a good tool to prepare a hematopoietic damage model. This animal model can be employed to study the hematopoietic efficacy of biologically active compounds.

• 한국식품과학회지
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• 제30권5호
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• pp.1222-1228
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• 1998

스트레스에 의해서 생체는 에너지 대사를 증가시키며, 에너지 대사의 증가는 높은 반응성의 ROS를 생성한다. ROS는 높은 반응성으로 인해 지질, 단백질 등을 과산화시켜 원래의 활성을 잃게함으로 이런 ROS에 대해서 높은 소거능을 지니고 흡수가 쉬운 SOD 유사물질의 투여가 스트레스로 인한 생체내 산화적 손상을 억제할 수 있을 것으로 생각된다. 이것을 확인하기위해서 실험용 흰 쥐에게 4주간의 고정화 스트레스를 가한 결과, 체중 증가량을 감소시켰으며 스트레스 호르몬의 하나인 5-HIAA의 수준을 증가시켰다. 시험관에서 높은 항산화력을 확인한 루이보스티 추출액을 스트레스를 받은 흰 쥐에게 투여한 결과는 체중 증가량 감소는 완화시켰으나 5-HIAA의 수준을 변화시키지 못하여 스트레스 반응 자체를 억제하지 않는 것으로 판명되었다. 루이보스티의 투여는 스트레스로 인해서 유도되는 뇌 조직의 지질과산화와 단백질 산화를 억제하였으나 SOD, GPx 등의 대표적 항산화 효소 활성의 변화를 유발하지 않았다. 따라서, 루이보스티는 스트레스 반응 자체보다는 그에 따른 2차적 독성 대사산물에 대해서 효소 활성의 증가가 아닌 루이보스티 추출액의 구성분 자체가 세포를 보호한 것으로 생각되며, 루이보스티의 추출액이 열수하에서 추출된 것이기 때문에 지질과산화에 대해서보다 단백질 과산화에 대해 더 높은 보호 활성이 나타난 것으로 생각된다.

• Journal of Ginseng Research
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• 제43권2호
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• pp.179-185
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• 2019

Background: Oxidative stress induces the production of reactive oxygen species (ROS), which play important causative roles in various pathological conditions. Black ginseng (BG), a type of steam-processed ginseng, has drawn significant attention due to its biological activity, and is more potent than white ginseng (WG) or red ginseng (RG). Methods: We evaluated the protective effects of BG extract (BGE) against oxidative stress-induced cellular damage, in comparison with WG extract (WGE) and RG extract (RGE) in a cell culture model. Ethanolic extracts of WG, RG, and BG were used to evaluate ginsenoside profiles, total polyphenols, flavonoid contents, and antioxidant activity. Using AML-12 cells treated with $H_2O_2$, the protective effects of WGE, RGE, and BGE on cellular redox status, DNA, protein, lipid damage, and apoptosis levels were investigated. Results: BGE exhibited significantly enhanced antioxidant potential, as well as total flavonoid and polyphenol contents. ATP levels were significantly higher in BGE-treated cells than in control; ROS generation and glutathione disulfide levels were lower but glutathione (GSH) and NADPH levels were higher in BGE-treated cells than in other groups. Pretreatment with BGE inhibited apoptosis and therefore protected cells from oxidative stress-induced cellular damage, probably through ROS scavenging. Conclusion: Collectively, our results demonstrate that BGE protects AML-12 cells from oxidative stress-induced cellular damages more effectively than WGE or RGE, through ROS scavenging, maintenance of redox status, and activation of the antioxidant defense system.

• Molecules and Cells
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• 제38권9호
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• pp.750-758
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• 2015

Genomic instability and altered metabolism are key features of most cancers. Recent studies suggest that metabolic reprogramming is part of a systematic response to cellular DNA damage. Thus, defining the molecules that fine-tune metabolism in response to DNA damage will enhance our understanding of molecular mechanisms of tumorigenesis and have profound implications for the development of strategies for cancer therapy. Sirtuins have been established as critical regulators in cellular homeostasis and physiology. Here, we review the emerging data revealing a pivotal function of sirtuins in genome maintenance and cell metabolism, and highlight current advances about the phenotypic consequences of defects in these critical regulators in tumorigenesis. While many questions should be addressed about the regulation and context-dependent functions of sirtuins, it appears clear that sirtuins may provide a promising, exciting new avenue for cancer therapy.