• Biomolecules & Therapeutics
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• 제23권6호
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• pp.582-589
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• 2015

Several theories emphasize that aging is closely related to oxidative stress and disease. The formation of excess ROS can lead to DNA damage and the acceleration of aging. Vigna angularis is one of the important medicinal plants in Korea. We isolated vitexin from V. angularis and elucidated the lifespan-extending effect of vitexin using the Caenorhabditis elegans model system. Vitexin showed potent lifespan extensive activity and it elevated the survival rates of nematodes against the stressful environments including heat and oxidative conditions. In addition, our results showed that vitexin was able to elevate antioxidant enzyme activities of worms and reduce intracellular ROS accumulation in a dose-dependent manner. These studies demonstrated that the increased stress tolerance of vitexin-mediated nematode could be attributed to increased expressions of stress resistance proteins such as superoxide dismutase (SOD-3) and heat shock protein (HSP-16.2). In this work, we also studied whether vitexin-mediated longevity activity was associated with aging-related factors such as progeny, food intake, growth and movement. The data revealed that these factors were not affected by vitexin treatment except movement. Vitexin treatment improved the body movement of aged nematode, suggesting vitexin affects healthspan as well as lifespan of nematode. These results suggest that vitexin might be a probable candidate which could extend the human lifespan.

• Anatomy and Cell Biology
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• 제56권1호
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• pp.16-24
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• 2023

Endothelial cells (EC) are the anatomical boundaries between the intravascular and extravascular space. Damage to ECs is catastrophic and induces endothelial cell dysfunction. The pathogenesis is multifactorial and involves dysregulation in the signaling pathways, membrane lipids ratio disturbance, cell-cell adhesion disturbance, unfolded protein response, lysosomal and mitochondrial stress, autophagy dysregulation, and oxidative stress. Autophagy is a lysosomal-dependent turnover of intracellular components. Autophagy was recognized early in the pathogenesis of endothelial dysfunction. Autophagy is a remarkable patho (physiological) process in the cell homeostasis regulation including EC. Regulation of autophagy rate is disease-dependent and impaired with aging. Up-regulation of autophagy induces endothelial cell regeneration/differentiation and improves the function of impaired ones. The paper scrutinizes the molecular mechanisms and triggers of EC dysregulation and current perspectives for future therapeutic strategies by autophagy targeting.

• Journal of Photoscience
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• 제9권2호
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• pp.146-149
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• 2002

Oxidative stress evoked hy Ultraviolet (UV) exposure has been suggested to be involved in UV-induced skin carcinogenesis. In this study, the role of oxidative stress in UV-carcinogenesis was evaluated by applying N-Acetylcysteine (NAC) in animal model of hairless-mouse. NAC is known to be a precursor of glutathione, which was converted to glutathione in cytoplasm, acting as an intracellular free radical scavenger. The glutathione levels in hairless mouse skin after one time application of NAC increased significantly. With and without the pre-treatment of NAC, hairless-mice were exposed to UVB three times a week, at total dose 274.4 kJ in 80 times, and the timing of tumor-development, incidence of skin tumor and the histopathology of tumors were observed. 8-hydroxy-2'-deoxyguanosine (8-0HdG), a typical form of oxidative damage in DNA has been also investigated in the course of experiment. The decrease of 8-0HdG formation of UVB- exposed skin compared to controls was observed in the early stage of experiment in the NAC-treated mice. In addition, initial tumor development delayed significantly in NAC-treated group. Finally the number of the tumor developed in the NAC-treated mice was fewer though not significant. These results suggest that antioxidants may have inhibitory effect in the initial step of UVB-induced carcinogenesis of hairless mice.

• 동의생리병리학회지
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• 제28권5호
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• pp.520-529
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• 2014

The purpose of this study is to investigate the protective effects of Yukmijiwhang-tang(YM) water extracts against the UVB irradiation on the human keratinocyte HaCaT cells. We observed the effects of YM on the oxidative stress, gene expression of pro-inflammatory cytokine such as TNF-${\alpha}$ and IL-$1{\beta}$, and matrix metalloproteinase-9 in UVB-irradiated HaCaT cells. On the effects of oxidative stress and antioxidant function on the treatment with YM, The activity of xanthine oxidase(XO) was significantly decreased by treatment of YM in all the concentrations(p<0.01). The activity of superoxide dismutase(SOD) and catalase(CAT) was significantly increased by treatment of YM in a dose dependent manner(p<0.05 and p<0.01). DPPH radical was erased by treatment of YM under dose of $500{\mu}g/m{\ell}$ concentration. Treatment of HaCaT cells with YM had also significantly reduced intracellular ROS produced by UVB irradiation in a dose dependent manner(p<0.05, p<0.01, p<0.001). Gelatin zymography assay showed that YM downregulated the MMP-9 activity in UVB-irradiated HaCaT cells. RT-PCR analysis revealed that YM suppressed the expression of IL-$1{\beta}$ and MMP-9 however, it has no effects on the expression of TNF-${\alpha}$ and MMP-3. Our study suggests that Yukmijiwhang-tang exert protective actions on the UVB-irradiated HaCaT cells largely by anti-oxidative and anti-inflammatory processes.

• Natural Product Sciences
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• 제12권1호
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• pp.1-7
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• 2006

We have screened the cytoprotective effect on ${\gamma}-ray$ radiation induced oxidative stress from forty one Korean plant extracts. Carpinus laxiflora (caulis), Quercus salicina (caulis), and Castanopsis cuspidata (caulis) were found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and intracellular reactive oxygen species (ROS). As a result, extracts of three plants reduced cell death of Chinese hamster lung fibroblast (V79-4) cells induced by $H_2O_2$ treatment. In addition, these extracts protected cell death of V79-4 cells damaged by ${\gamma}-ray$ radiation. In addition, these extracts scavenged ROS generated by radiation. Taken together, the results suggest that Carpinus laxiflora, Quercus salicina, and Castanopsis cuspidata protect V79-4 cells against oxidative damage by radiation through scavenging ROS.

• 대한한의학회지
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• 제39권1호
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• pp.35-43
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• 2018

Objectives: In the brain, glutamate is the most important excitable neurotransmitter in physiological and pathological conditions. However, the high level of glutamate induces neuronal cell death due to exitotoxicity and oxidative stress. The present study investigated to evaluate a possible neuroprotective effect of furosin isolated from Euphorbia helioscopia against glutamate-induced HT22 cell death. Methods: Furosin was isolated from methanol extract of Euphorbia helioscopia and examined whether it protects glutamate-induced neuronal cell death. The cell viability was determined using Ez-Cytox assay. Anti-oxidative effect of furosin was determined by DPPH scavenging activities, and the levels of intracellular reactive oxygen species (ROS) were determined by the fluorescent intensity after staining the cells with $H_2DCFDA$. To evaluate apoptotic cell death, we performed nuclear staining and image-based cytometeric analysis. Results: The cell viability was significantly increased by treatement with furosin compared with the treatment with glutamate. Furosin showed a strong DPPH radical scavenging activity ($EC50=1.83{\mu}M$) and prevented the accumulation of intra cellular ROS. Finally, the presence of 50 and $100{\mu}M$ furosin significantly the percentage of apoptotic cells compared with glutamate treatment. Conclusion: The present study found that furosin is a potent neuroprotectant against glutamate-induced oxidative stress through inhibition of apoptotic cell death induced by glutamate. Therefore, the present study suggests that furosin as a bioactive compound of E. helioscopia can be a useful source to develop a drug for the treatment of neurodegenerative diseases and acute brain injuries.

• Biomolecules & Therapeutics
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• 제21권4호
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• pp.270-276
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• 2013

Fucoxanthin is an important carotenoid derived from edible brown seaweeds and is used in indigenous herbal medicines. The aim of the present study was to examine the cytoprotective effects of fucoxanthin against hydrogen peroxide-induced cell damage. Fucoxanthin decreased the level of intracellular reactive oxygen species, as assessed by fluorescence spectrometry performed after staining cultured human HaCaT keratinocytes with 2',7'-dichlorodihydrofluorescein diacetate. In addition, electron spin resonance spectrometry showed that fucoxanthin scavenged hydroxyl radical generated by the Fenton reaction in a cell-free system. Fucoxanthin also inhibited comet tail formation and phospho-histone H2A.X expression, suggesting that it prevents hydrogen peroxide-induced cellular DNA damage. Furthermore, the compound reduced the number of apoptotic bodies stained with Hoechst 33342, indicating that it protected keratinocytes against hydrogen peroxide-induced apoptotic cell death. Finally, fucoxanthin prevented the loss of mitochondrial membrane potential. These protective actions were accompanied by the down-regulation of apoptosis-promoting mediators (i.e., B-cell lymphoma-2-associated ${\times}$ protein, caspase-9, and caspase-3) and the up-regulation of an apoptosis inhibitor (B-cell lymphoma-2). Taken together, the results of this study suggest that fucoxanthin defends keratinocytes against oxidative damage by scavenging ROS and inhibiting apoptosis.

• Journal of Radiation Protection and Research
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• 제31권3호
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• pp.115-122
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• 2006

We have screened the cytoprotective effect on $\gamma$-ray radiation induced oxidative stress from eighteen Korean plant extracts. Querus salicina, Clerodendron trichotomum, Lamium amplexicaule, Lozoste lancifolia and Malus baccata were found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and intracellular reactive oxygen species (ROS). As a result, extracts of these plants reduced cell death of Chinese hamster lung fibroblast (V79-4) cells induced by $H_2O_2$ treatment. In addition, these extracts protected cell death of V79-4 cells damaged by $\gamma$-ray radiation. In addition, these extracts scavenged ROS generated by radiation. Taken together, the results suggest that Quercus salicina, Clerodendron trichotomum, Lamium amplexicaule, Lozoste lancifolia and Malus baccata protect V79-4 cells against oxidative damage by radiation through scavenging ROS.

• 대한통합의학회지
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• 제11권4호
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• pp.73-82
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• 2023

Purpose : Cymbopogon citratus, also known as lemongrass, has widely spread around the world and its essential oil is usually applied in food, perfume, and other industrial purposes. In addition, C. citratus has also been used for the treatment of inflammation, digestive disorders, and diabetes in traditional medicine. In this study, the antioxidative activity of C. citratus ethanol extract (CCEE) was analyzed in RAW 264.7 cells through the induction of one of phase II enzymes, heme oxygenase (HO)-1 by nuclear factor-erythroid 2 p45-related factor (Nrf)2, mitogen-activated protein kinase (MAPK), and phosphoinositide 3-kinase (PI3K)/Akt. Methods : The antioxidative activity of CCEE against oxidative stress and its underlying molecular mechanisms were analyzed by the cell viability assay, intracellular reactive oxygen species (ROS) formation assay, and Western blot analysis in RAW 264.7 cells. Results : The results exhibited that CCEE potently attenuated tert-butyl hydroperoxide (t-BHP) induced intracellular ROS levels in a dose-dependent manner without any cytotoxicity. CCEE treatment significantly induced the expression of HO-1 which is known for its antioxidative capacity. In addition, CCEE treatment significantly upregulated the expression of Nrf2, a corresponding transcription factor for the regulation of antioxidative enzymes, which was in accordance with the HO-1 overexpression. MAPK and PI3K/Akt were also evaluated for their important roles in the regulation of cellular redox homeostasis against oxidative damage. As a result, the potent HO-1 expression was mediated by not extracellular regulated kinase (ERK), c-Jun NH2 terminal kinase (JNK), p38, but phosphoinositide 3-kinase (PI3K) phosphorylation. To confirm the antioxidative activity of CCEE-induced HO-1 expression, oxidative damage was initiated by t-BHP and attenuated by CCEE treatment, which was identified by HO-1 selective inhibitor and inducer. Conclusion : Consequently, CCEE potently induced the HO-1-mediated antioxidative potential through the modulation of Nrf2 and PI3K/Akt signaling pathways in RAW 264.7 cells. These results suggest that CCEE could be a promising strategy for the mitigation against cellular oxidative damage.

• Journal of Photoscience
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• 제9권2호
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• pp.482-484
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• 2002

UV irradiation activates various intracellular signaling pathways causing cell death in a DNA damage-dependent and an independent manner. As DNA photoproducts, major forms of DNA damage, are maximally formed by UV light at 260-nm, short wavelength UV (UVC) is more harmful than middle wavelength UV (UVB). However, the differences or similarities in responses of DNA damage-independent intracellular signaling molecules to UVB and UVC are not elucidated. We examined activation of signaling molecules towards apoptosis in normal human fibroblastic cells after irradiation with UVB or UVC at a dose generating the equal amount of DNA photoproducts. Both UVB and UVC induced transient phosphorylation of ERK and sustained phosphorylation of p38. Phosphorylation of p53 at Ser15 and at Ser392 residues were also observed, which were inhibited by a phosphoinositide 3-kinase inhibitor, wortmannin. In contrast, an antioxidant N-acetyl-cysteine and a p38 inhibitor SB203580 suppressed only Ser392 phosphorylation, suggesting that UV-induced oxidative stress and p38 activation were involved in the phosphorylation of this site. The apoptic signals such as mitochondrial cytochrome C release and annexin V binding were then observed. Overall, no difference was found in chronological responses of p53, MAPK, and apoptosis between UVB-irradiated and UVC-irradiated cells. These results suggested that DNA damage-independent intracellular signaling molecules similarly responded to UVB and UVC when the equal level of DNA photoproducts were generated.