• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.137-137
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• 2002

Capsaicin has been reported to induce apoptosis in various cancer cells. However, its effect on bladder cancer cells has not been studied. In this study, we investigated whether capsaicin induces apoptosis in murine orthotopic bladder cancer MBT-2 cells and reactive oxydative species(ROS) are involved in capsaicin-induced apoptotic process.(omitted)

• YAKHAK HOEJI
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• v.45 no.1
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• pp.78-84
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• 2001

Heme oxygenase is a rate-limiting enzyme in heme catabolism that cleaves heme to form biliverdin, iron, and carbon monoxide. Heme oxygenase-1 is expressed in many types of cells and tissues and is highly induced in response to oxidative stress. Carbon monoxide, one of the products of heme oxygenase, can stimulate soluble guanylate cyclase and dilate the vascular smooth muscle. So, the induction of heme oxygenase by lipopolysaccharide (LPS)-induced oxydative stress and the effect of the resultant carbon monoxide on aortic contractility were examined in this study. Zinc protoporphyrine IX (ZnPP), a inhibitor of heme oxygenase, elicited weak contraction of thoracic aortic ring, and this effect was more potent in aorta of LPS-treated rats than control and was blocked by methylene blue. The hyperreactivity to ZnPP in LPS-treated group was blocked by co-treatment with aminoguanidine. In the aortic ring of LPS-treated rats, ZnPP didn't change the vasoreactivity to phenylephrine or acetylcholine. ZnPP elicited hyper-tensive effect in concious rats, and pretreatment with LPS did not affect this effect. Prazosin significantly diminished the hypertensive effect of ZnPP. These results indicate that LPS induced heme oxygenase in aotra, and the resultant carbon monoxide diminished the aortic reactivity to vasoconstrictor.

• Journal of Life Science
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• v.10 no.4
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• pp.354-361
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• 2000

The effect of mulberry (Morus alba L.) leaf extract(MLE) on oxidative stress and membrane fluidity in brain membranes of SD rats fed with 100 and 300 mg/kg BW/day were carried out for 6 weeks. Cholesterol accumulations resulted in a consistent decreases (4.6% and 5.6%, respectively) in brain mitochondria and microsomes of MLE-300 group compared with control group. Membrane fluidities were dose-dependently increased (2.2% and 5.1%, 5.0% and 15.2%) in brain mitochondria and microsomes of MLE-100 and MLE-300 groups compared with control group. Basal oxygen radicals(BORs) in brain mitochondria and microsomes were significantly inhibited (15.7% and 25.1%, 9.0% and 12.4%, respectively) by MLE-100 and MLE-300 groups compared with control group. Induced oxygen radicals(IORs) in brain mitochondria and microsomes were significantly inhibited (8.9% and 13.1%, 16.5% and 23.2%, respectively) by MLE-100 and MLE-300 groups compared with control group. Lipid peroxide (LPO) levels were significantly decreased (8.5% and 18.1%, 7.6% and 12.3%) in brain mitochondria and microsomes of MLE-100 and MLE-300 groups compared with control group. Oxidized protein (OP) levels were dose-dependently decreased (4.3% and 14.2%, 10.0% and 10.9%, respectively) in brain microsomes of MLE-100 and MLE-300 groups compared with control group. These results suggest that MLE may play an effective role in an attenuating an oxidative stress and increasing a membrane fluidity in brain membranes.

• Physical Therapy Rehabilitation Science
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• v.3 no.1
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• pp.33-37
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• 2014

Objective: Low intensity pulsed ultrasound (LIPUS) has been shown to accelerate cell proliferation and tissue healing in both animal models and clinical trials. However, details of the clinical effects of LIPUS have not been well characterized. The aim of this study was to investigate the effect of LIPUS on mitogen-activated protein kinase (MAPK) activation in rat articular chondrocytes. Design: Cross-sectional study. Methods: Chondrocyte were cultured in six well cell culture plates for 72 hours at $37^{\circ}C$ with 5% $CO_2$, and then exposed to LIPUS at 1.5 MHz frequency and $30-mW/cm^2$ power. Changes in chondrocyte activities were evaluated in response to oxydative stress in dose-dependent (0 and 300 uM) and time-dependent (0-24 hr) manner. The cell viability were analyzed using MTT [3-(4.5-dimethylthiazol-2-yl)-2.5 diphenyltetrazolium bromide]. The expression of p38 MAPK was measured using western blotting. Results: Oxidative stress was induced in rat chondrocytes using hydrogen peroxide ($H_2O_2$). The cell viability was decreased in chondrocytes after the $H_2O_2$ dose and time-dependent treatment. The p38 MAPK phosphorylation occurred at a significantly increased rate after $H_2O_2$ treated (p<0.05). Expression of p38 MAPK was decreased in the p38 inhibitor groups compared with the oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways (p<0.05). Conclusions: It could be concluded that LIPUS can inhibit oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways.

• Journal of Microbiology and Biotechnology
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• v.26 no.2
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• pp.277-286
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• 2016

Makgeolli lees (ML) has several physiological effects such as antioxidant, antidiabetic, and anticancer properties, but its biological functions have not been determined definitively. Here, we tested whether ML has a cytoprotective effect on paraquat (PQ)-induced oxidative stress in the human lung carcinoma cell line A549. At 0.1 mg/ml ML, viability of PQ-exposed A549 cells was restored by 12.4%, 18.5%, and 48.6% after 24, 48, and 72 h, respectively. ML also reduced production of the intracellular reactive oxygen species (ROS) that were generated by PQ treatment. Further experiments revealed that ML treatment enhanced the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) as well as ARE-GFP reporter activity. ML treatment also effectively increased the expression of NRF2's target genes NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase 1 (HO-1). Moreover, we found that expression of cytoprotective genes, including glutathione peroxidases (GPXs), superoxide dismutase (SOD1), catalase (CAT), peroxiredoxin 3 (PRDX3), and peroxiredoxin 4 (PRDX4), was greatly enhanced by treatment with ML during PQ exposure. Taken together, the data suggest that treatment of PQ-exposed A549 cells with ML ameliorates cytotoxicity through induction of NRF2 expression and its target genes HO-1, NQO1, and other antioxidant genes. Thus, ML may serve as a functional food applicable to ROS-mediated human diseases.