• Proceedings of the Korean Society of Applied Pharmacology
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• 2004.04a
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• pp.3-10
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• 2004

Oxidative stress is a constant threat to all living organisms and an immense repertoire of cellular defense systems is being employed by most pro- and eukaryotic systems to eliminate or to attenuate oxidative stress. Ischemia and reperfusion is characterized by both a significant oxidative stress and characteristic changes in the antioxidant defense. Heme oxigenase-l (HO-l) is up-regulated by various stimuli including oxidative stress so that it is thought to participate in general cellular defense mechanisms against ischemic injury in mammalian cells. Higenamine, an active ingredient of Aconite tuber, has been shown to have antioxidant activity along with inhibitory action of inducible nitric oxide synthase (iNOS) expression in various cells. In the present study, we investigated whether higenamine and related analogs protect cells from oxidative cellular injuries by modulating antioxidant enzymes, such as HO-l, MnSOD etc. R-form of YS-51 was the most potent inducer of HO-l in bovine endothelial cells, which inhibited apoptotic cell death by H$_2$O$_2$. HO-1 induction by YS 51 was mediated by PI3 kinase activation in which PKA- as well as PKG pathway is considered as important regulators. YS-51 also induced Mn-SOD mRNA expression by activating c-jun N-terminal kinase in endothelial cells and Hela cells. In ROS 17/2.1 cells, higenamine and enetiomers of related compounds inhibited iNOS expression by cytokine mixtures. Taken together, higenamine and related compounds can be developed as possible protective agents from oxidative cell injury or death.

• Parasites, Hosts and Diseases
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• v.50 no.4
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• pp.375-377
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• 2012

Malaria is still a leading cause of morbidity and mortality. The increase in lipid peroxidation reported in malaria infection and antioxidant status may be a useful marker of oxidative stress during malaria infection. The aim of this study was to investigate the role of antioxidant enzymes against toxic reactive oxygen species in patients infected with Plasmodium vivax and healthy controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were determined in 91 P. vivax patients and compared with 52 controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were $8.07{\pm}2.29$ nM/ml, $2.69{\pm}0.33$ U/ml, and $49.6{\pm}3.2$ U/g Hb in the patient group and $2.72{\pm}0.50$ nM/ml, $3.71{\pm}0.47$ U/ml, and $62.3{\pm}4.3$ U/g Hb in the control group, respectively. Malondialdehyde levels were found statistically significant in patients with vivax malaria higher than in healthy controls (P<0.001). On the other hand, superoxide dismutase and glutathione peroxidase activities were found to be significantly lower in vivax malaria patients than in controls (P<0.05). There was an increase in oxidative stress in vivax malaria. The results suggested that antioxidant defense mechanisms may play an important role in the pathogenesis of P. vivax.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.33 no.4
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• pp.32-43
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• 2020

Objectives : The aim of this study was to investigate the anti-oxidant and anti-aging effect of the seed of Camellia japonica L. extracted by supercritical CO₂. Methods : The cell viability was performed by MTT assay. Nitric oxide (NO) production was performed by NO assay. The anti-oxidant effect was performed by beta-carotene bleaching assay and the intracellular proteome was analyzed expression of each 15 proteins by 2-D electrophoresis. Results : Fatty acid analysis of extract from Camellia japonica L. has shown oleic acid was 84%. And the antioxidant effect was about 186% compared with alpha-tocoperol(0.1%) by beta carotene bleaching assay. In 2D PAGE analysis, fifteen protein changes in five mechanisms which was collagen synthesis pathway, MMPs, ECM-cell interaction, cytokine, antioxidant enzymes were analyzed. Conclusions : On this study extract from seed of Camellia japonica L. by supercritical extraction could be used as a antioxidant and antiaging substance for the skin.

• Journal of The Korean Society of Clinical Toxicology
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• v.15 no.2
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• pp.107-115
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• 2017

Purpose: Glehnia littoralis has been used to treat ischemic stroke, phlegm, cough, systemic paralysis, antipyretics and neuralgia. The pharmacological mechanisms of Glehnia littoralis include calcium channel block, coumarin derivatives, anticoagulation, anti-convulsive effect, as well as anti-oxidant and anti-inflammatory effects. Alpha-amanitin (${\alpha}$-amanitin) is a major toxin from extremely poisonous Amanita fungi. Oxidative stress, which may contribute to severe hepatotoxicity was induced by ${\alpha}$-amanitin. The aim of this study was to investigate whether Glehnia littoralis ethyl acetate extract (GLEA) has the protective antioxidant effects on ${\alpha}$-amanitin -induced hepatotoxicity. Methods: Human hepatoma cell line HepG2 cells were pretreated in the presence or absence of GLEA (50, 100 and $200{\mu}g/ml$) for 4 hours, then exposed to $60{\mu}mol/L$ of${\alpha}$-amanitin for an additional 4 hours. Cell viability was evaluated using the MTT method. AST, ALT, and LDH production in a culture medium and intracellular MDA, GSH, and SOD levels were determined. Results: GLEA (50, 100 and $200{\mu}g/ml$) significantly increased the relative cell viability by 7.11, 9.87, and 14.39%, respectively, and reduced the level of ALT by 10.39%, 34.27%, and 52.14%, AST by 9.89%, 15.16%, and 32.84%, as well as LDH by 15.86%, 22.98%, and 24.32% in culture medium, respectively. GLEA could also remarkably decrease the level of MDA and increase the content of GSH and SOD in the HepG2 cells. Conclusion: In the in vitro model, Glehnia littoralis was effective in limiting hepatic injury after ${\alpha}$-amanitin poisoning. Its antioxidant effect is attenuated by antidotal therapy.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.80-84
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• 2008

Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

• Journal of Microbiology and Biotechnology
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• v.32 no.8
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• pp.989-1002
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• 2022

Cephalopods, in particular octopus (Octopus vulgaris), have the ability to alter their appearance or body pattern by showing a wide range of camouflage by virtue of their chromatophores, which contain nanostructured granules of ommochrome pigments. Recently, the antioxidant and antimicrobial activities of ommochromes have become of great interest; therefore, in this study, the pH-dependent redox effect of the extraction solvent on the antioxidant potential and the structural characterization of the pigments were evaluated. Cell viability was determined by the microdilution method in broth by turbidity, MTT, resazurin, as well as fluorescence microscopy kit assays. A Live/Dead Double Staining Kit and an ROS Kit were used to elucidate the possible inhibitory mechanisms of ommochromes against bacterial and fungal strains. The results obtained revealed that the redox state alters the color changes of the ommochromes and is dependent on the pH in the extraction solvent. Natural phenoxazinone (ommochromes) is moderately toxic to the pathogens Staphylococcus aureus, Bacillus subtilis, Salmonella Typhimurium and Candida albicans, while the species Pseudomonas aeruginosa and Pseudomonas fluorescens, and the filamentous fungi Aspergillus parasiticus, Alternaria spp. and Fusarium verticillioides, were tolerant to these pigments. UV/visible spectral scanning and Fourier- transform infrared spectroscopy (FTIR) suggest the presence of reduced ommatin in methanol/ HCl extract with high intrinsic fluorescence.

• The Korean Journal of Pain
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• v.35 no.3
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• pp.271-279
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• 2022

Background: Inflammation is known to underlie the pathogenesis in neuropathic pain. This study investigated the anti-inflammatory and neuroprotective mechanisms involved in antinociceptive effects of co-administration of acetaminophen and L-carnosine in chronic constriction injury (CCI)-induced peripheral neuropathy in male Wistar rats. Methods: Fifty-six male Wistar rats were randomly divided into seven experimental groups (n = 8) treated with normal saline/acetaminophen/acetaminophen + L-carnosine. CCI was used to induce neuropathic pain in rats. Hyperalgesia and allodynia were assessed using hotplate and von Frey tests, respectively. Investigation of spinal proinflammatory cytokines and antioxidant system were carried out after twenty-one days of treatment. Results: The results showed that the co-administration of acetaminophen and L-carnosine significantly (P < 0.001) increased the paw withdrawal threshold to thermal and mechanical stimuli in ligated rats compared to the ligated naïve group. There was a significant (P < 0.001) decrease in the levels of nuclear factor kappa light chain enhancer B cell inhibitor, calcium ion, interleukin-1-beta, and tumour necrotic factor-alpha in the spinal cord of the group coadministered with acetaminophen and L-carnosine compared to the ligated control group. Co-administration with acetaminophen and L-carnosine increased the antioxidant enzymatic activities and reduced the lipid peroxidation in the spinal cord. Conclusions: Co-administration of acetaminophen and L-carnosine has anti-inflammatory effects as a mechanism that mediate its antinociceptive effects in CCI-induced peripheral neuropathy in Wistar rat.

• Journal of The Korean Society of Grassland and Forage Science
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• v.42 no.4
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• pp.222-228
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• 2022

This study was conducted to investigate the effect of waterlogging stress on the physiological response and growth characteristics of the five Italian ryegrass varieties. For all varieties, the germination rate of seed decreased by 10-15% as the waterlogging period increased, but the waterlogging stress treatment after the early seedling stage increased the growth of shoot and root length. Photosynthetic activity (Fv/Fm) according to waterlogging stress treatment decreased in all vareity, and Florida 80 showed the least decrease with 1.5%. Waterlogging stress treatment was found to reduce the accumulation of reactive oxygen species (malondialdehyde, MDA) and the activities of antioxidant enzymes. These results suggest that other mechanisms may be involved in the defense mechanism of Italian ryegrass against waterlogging stress, such as promoting root growth to escape from waterlogging stress, in addition to the antioxidant enzyme system.

• Food Science of Animal Resources
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• v.43 no.4
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• pp.612-624
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• 2023

The gut-brain axis encompasses a bidirectional communication pathway between the gastrointestinal microbiota and the central nervous system. There is some evidence to suggest that probiotics may have a positive effect on cognitive function, but more research is needed before any definitive conclusions can be drawn. Inflammation-induced by lipopolysaccharide (LPS) may affect cognitive function. To confirm the effect of probiotics on oxidative stress induced by LPS, the relative expression of antioxidant factors was confirmed, and it was revealed that the administration of probiotics had a positive effect on the expression of antioxidant-related factors. After oral administration of probiotics to mice, an intentional inflammatory response was induced through LPS i.p., and the effect on cognition was confirmed by the Morris water maze test, nitric oxide (NO) assay, and interleukin (IL)-1β enzyme-linked immunosorbent assay performed. Experimental results, levels of NO and IL-1β in the blood of LPS i.p. mice were significantly decreased, and cognitive evaluation using the Morris water maze test showed significant values in the latency and target quadrant percentages in the group that received probiotics. This proves that intake of these probiotics improves cognitive impairment and memory loss through anti-inflammatory and antioxidant mechanisms.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4405-4409
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• 2014

Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.