• Molecules and Cells
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• v.38 no.3
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• pp.229-235
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• 2015

Nicotinamide (NAM) has been shown to suppress reactive oxygen species (ROS) production in primary human fibroblasts, thereby extending their replicative lifespan when added to the medium during long-term cultivation. Based on this finding, NAM is hypothesized to affect cellular senescence progression by keeping ROS accumulation low. In the current study, we asked whether NAM is indeed able to reduce ROS levels and senescence phenotypes in cells undergoing senescence progression and those already in senescence. We employed two different cellular models: MCF-7 cells undergoing senescence progression and human fibroblasts in a state of replicative senescence. In both models, NAM treatment substantially decreased ROS levels. In addition, NAM attenuated the expression of the assessed senescence phenotypes, excluding irreversible growth arrest. N-acetyl cysteine, a potent ROS scavenger, did not have comparable effects in the tested cell types. These data show that NAM has potent antioxidative as well as anti-senescent effects. Moreover, these findings suggest that NAM can reduce cellular deterioration caused by oxidative damage in postmitotic cells in vivo.

• Korean Journal of Pharmacognosy
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• v.33 no.3 s.130
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• pp.252-256
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• 2002

In the previous study, we demonstrated that ginsenoside $Rb_1$ isolated from the butanol fraction of the head of Panax ginseng had significant gastroprotective activity on gastritis and gastric ulcer models in rats. It has been well established that drugs to have capacity of scavenging or inhibiting the generation of reactive oxygen radicals prevent the gastric mucosal injury. Ginsenoside $Rb_1$ was tested on HCl ethanol-induced gastritis in rats, DPPH-induced free radical scavenging effect, MDA assay, GSH activity, and SOD activity in gastric tissue. It showed significant inhibition in HCl ethanol-induced gastritis, and al~o significantly increase of GSH activated SOD. We speculate that the protective effect of ginsenoside $Rb_1$ against HCl ethanol-induced gastric mucosal damage is originated from the increase of GSH and the activation of SOD.

• Archives of Plastic Surgery
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• v.41 no.1
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• pp.35-39
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• 2014

Background Aurora kinase A (Aurora-A) plays an important role in the regulation of mitosis and cytokinesis. Dysregulated Aurora-A leads to mitotic faults and results in pathological conditions. No studies on Aurora-A expression in human diabetic skin tissue have been reported. In light of this, we explored the expression of Aurora-A in human diabetic skin tissue. Methods Aurora-A protein was evaluated by western blotting in 6 human diabetic skin tissue and 6 normal skin specimens. Results Increased expression of Aurora-A protein was detected in all diabetic skin tissue samples in both western blot analysis and immunohistochemical staining. However, in the case of the normal skin tissue, no bands of Aurora-A protein were detected in either the western blotting analysis or the immunohistochemical staining. Conclusions Thus far, there have been no studies on the expression of Aurora-A in diabetic skin tissue. However, we believe that oxidative DNA damage related to the expression of Aurora-A protein and Aurora-A could be involved inhuman diabetic skin tissue.

• Advances in Traditional Medicine
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• v.3 no.4
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• pp.205-211
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• 2003

Stem bark of Cinchona sp. (Rubiaceae) is one of the well known drugs for its therapeutic values in traditional as well as modern medicine. Even though a lot of work has been carried out on quinoline alkaloids of Cinchona, its phenolic constituents received very little attention. In the present study, we evaluated antioxidant properties of C. officinalis stem bark methanolic extract and water extract containing phenolic compounds (total phenolics 21.37, 5.18% w/w respectively in the two extracts) in different in vitro and ex vivo models viz., antiradical activity by DPPH reduction, superoxide radical scavenging activity in riboflavin/light/NBT system, nitric oxide radical scavenging activity in sodium nitroprusside/Greiss reagent system and inhibition of lipid peroxidation induced by iron-ADP-ascorbate in liver homogenate and haemolysis of erythrocytes induced by phenylhydrazine in erythrocyte membrane stabilization study. Both the extracts exhibited very good antioxidant activity in all the models tested. The phenolic compounds including tannins present in the stem bark seem to offer protection from the oxidative damage.

• YAKHAK HOEJI
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• v.44 no.3
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• pp.237-244
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• 2000

Liver isolated from 18 hours fasted rats was subjected to $N_2$hypoxia (for 45 min) followed by reoxygenation (for 30 min). The perfusion medium used was Krebs-Henseleit bicarbonate buffer (pH 7.4, $37^{\circ}C$). Vitamin C (0.5 mM) and trolox C (0.5 mM), soluble vitamin E analog, were added to perfusate. Lactate dehydrogenase (LDH), total glutathione, oxidized glutathione, lipid peroxide and drug-metabolizing enzymes were measured. After hypoxia LDH significantly increased but this increase was attenuated by vitamin C and combination of vitamin C and E. Total glutathione and oxidized glutathione in perfusate markedly increased during hypoxia and this increase was inhibited by vitamins C, E and its combination. Similarly; oxidized glutathione and lipid peroxide in liver tissue increased after hypoxia and reoxygenation and this increase was inhibited by vitamin I and combination of vitamin C and E. Hepatic drug metabolizing function (phase I, II) were suppressed during hypoxia but improved during reoxygenation. While vitamins C and E only increased glucuronidation, the combination of vitamin C and E increased the oxidation, glucuronidation and sulfation. Our findings suggest that vitamins C and E synergistically ameliorates hepatocellular damage as indicated by abnormalities in drug metabolizing function during hypoxia/reoxygenation and that this protection is in major part, caused by decreased oxidative stress.

• KSBB Journal
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• v.19 no.1
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• pp.67-71
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• 2004

An antioxidant activity of Rosa rugosa extract and its solvent-partitioned fractions was determined not only by measuring lipid peroxide produced when a mouse liver homogenate was exposed to the air at 37$^{\circ}C$, using thiobarbituric acid (TBA) but also by evaluating the free radical scavenging effect against DPPH radical, authentic peroxynitrite, and 3-morpholinsydnonimine (SIN-1). All its partitioned fractions including crude extract showed potent scavenging effect against DPPH radical, peroxynitrite, and lipid peroxidation. n-BuOH fraction, in particular, was found to be the most effective in DPPH radical scavenging ability as well as inhibition against lipid peroxidation. The 15% aqueous MeOH fraction also showed a strong potency which was slightly lower than n-BuOH fraction. Based on these results, we suggest that Rosa rugosa could be useful for preventing an oxidative damage.

• BMB Reports
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• v.31 no.6
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• pp.572-577
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• 1998

A soluble protein from Saccharomyces cerevisiae provides protection against a thiol-containing oxidation system but not against an oxidation system without thiol. This 25-kDa protein acts as a peroxidase but requires the NADPH-dependent thioredoxin system or a thiol-containing intermediate, and was thus named thioredoxin peroxidase. The protective role of thioredoxin peroxidase against ionizing radiation, which generates reactive oxygen species harmful tocellular function, was investigated in wild-type and mutant yeast strains in which the tsa gene encoding thioredoxin peroxidase was disrupted by homologous recombination. Upon exposure to ionizing radiation, there was a distinct difference between these two strains in regard to viability and the level of protein carbonyl content, which is the indicative marker of oxidative damage to protein. Activities of other antioxidant enzymes, such as catalase, superoxide dismutase, glucose-6-phosphate dehydrogenase, and glutathione reductase were increased at 200-600 Gy of irradiation in wild-type cells. However, the activities of antioxidant enzymes were not significantly changed by ionizing radiation in thioredoxin peroxidase-deficient mutant cells. These results suggest that thioredoxin peroxidase acts as an antioxidant enzyme in cellular defense against ionizing radiation through the removal of reactive oxygen species as well as in the protection of antioxidant enzymes.

• BMB Reports
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• v.47 no.2
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• pp.51-59
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• 2014

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.

• Journal of Pharmacopuncture
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• v.6 no.1
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• pp.67-72
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• 2003

Bee venom has been clinically used to control the pain of inflammation disease etc. in general. Although the effect of bee venom herbal acupuncture has been reported, its mechanism has not been fully elucidated yet. Free radical metabolism seems to occupy a remarkably common position in the mechanisms of inflammation and ageing related disease. Oxidative damage to DNA, lipids, proteins and other molecules may contribute to the development inflammation disease. NO or DPPH is one of the free radicals and a mediator in inflammation diseases. The objective of this study is to investigate the scavenging effect of bee venom herbal acupuncture against NO and DPPH. The followings are the summary of the results: (1) There is no significant scavenging effect of bee venom herbal acupuncture on NO in BVS and BVP group. (2) There is a significant scavenging effect of bee venom herbal acupuncture on DPPH in BVS-1 and BVP-1 group. These results suggest that bee venom herbal acupuncture can be used for inflammation diseases such as rheumatoid arthritis. This study would provide important basic data on the possibility of the clinical treatment of bee venom herbal acupuncture. Further studies are required to investigate the antioxidative effects of it.

• The Plant Pathology Journal
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• v.34 no.4
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• pp.335-340
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• 2018

To investigate the difference in the disinfectant efficiency of ozone microbubbles ($O_3MB$) and ozone millibubbles ($O_3MMB$), the morphological change of the treated Fusarium oxysporum f. sp. melonis spores was observed with scanning and transmission electron microscopies (SEM and TEM). The disinfectant efficiency of $O_3MB$ on F. oxysporum f. sp. melonis spores was greater than that of $O_3MMB$. On observation with SEM, it was revealed that morphological change of F. oxysporum f. sp. melonis spores was caused by $O_3MB$ and $O_3MMB$, and damage to the spore surfaces by $O_3MB$ occurred sooner than that by $O_3MMB$. On observation with TEM, it was furthermore confirmed that F. oxysporum f. sp. melonis spores treated with $O_3MB$ induced wavy deformation of cell membrane and the intracellular change different from that with $O_3MMB$. Therefore, the greater disinfection efficiency of $O_3MB$ was suggested to be caused due to the function of the MB in addition to the oxidative power of $O_3$.