• The Korea Journal of Herbology
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• v.28 no.6
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• pp.79-86
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• 2013

Objectives : The purpose of this study is to investigate neuroprotective effects and molecular mechanisms of luteolin against ${\beta}$-amyloid ($A{\beta}_{25-35}$)-induced oxidative cell death in BV-2 cells. Methods : The protective effects of luteolin against $A{\beta}_{25-35}$-induced cytotoxicity and apoptotic cell death were determined by MTT dye reduction assay and TUNEL staining, respectively. The apoptotic cell death was further analyzed by measuring mitochondrial transmembrane potential and expression of pro- and/or anti-apoptotic proteins. To elucidate the molecular mechanisms underlying the protective effects of luteolin, intracellular accumulation of reactive oxygen species, oxidative damages, and expression of antioxidant enzymes were examined. Results : Luteolin pretreatment effectively attenuated $A{\beta}_{25-35}$-induced apoptotic cell death indices such as DNA fragmentation, dissipation of mitochondrial transmembrane potential, increased Bax/Bcl-2 ratio, and activation of c-Jun N-terminal kinase and caspase-3 in BV-2 cells. Furthermore, $A{\beta}_{25-35}$-induced intracellular formation of reactive oxygen species and subsequent oxidative damages such as lipid peroxidation and depletion of endogenous antioxidant glutathione were suppressed by luteolin treatment. The neuroprotective effects of luteolin might be mediated by up-regulation of cellular antioxidant defense system via up-regulation of ${\gamma}$-glutamylcysteine ligase, a rate-limiting enzyme in the glutathione biosynthesis and superoxide dismutase, an enzyme involved in dismutation of superoxide anion into oxygen and hydrogen peroxide. Conclusions : These findings suggest that luteolin has a potential to protect against $A{\beta}_{25-35}$-induced neuronal cell death and damages thereby exhibiting therapeutic utilization for the prevention and/or treatment of Alzheimer's disease.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.6
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• pp.3663-3667
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• 2013

Background: Multiple myeloma is a malignant silent incurable plasma cell disorder. The present study aimed to assessed the activation of the oxidative stress pathway in afected patients Materials and Methods: Advanced oxidation protein products (AOPPs), malondialdehyde (MDA), adenosine deaminase (ADA), total antioxidant capacity (TAC) levels, glutathione, ascorbic acid (vitamin C), ${\alpha}$-tocopherol (vitamin E) in addition to related enzymes glutathione peroxidase (GSH-Px), glutathione reductase (GSH-R) and superoxide dismutase (SOD) were analyzed in sixty patients with multiple myeloma before and after one month treatment with induction therapy. Results: The results of the study showed a significant elevation in AOPPs, MDA, ADA levels in patients with multiple myeloma before and after treatment in comparison to healthy control samples In contrast TAC glutathione, vitamin C and E, and the antioxidant enzymes levels were decreased significantly. On comparing samples of MM patients after treatment, there was significant increase of TAC glutathione, vitamin C and E, and the antioxidant enzymes in parallel with decreasing AOPPs, MDA and ADA levels in comparison with samples of patients before treatment. Conclusions: The results indicate oxidative stress and DNA damage activity increase in MM and are alleviated in response to therapy.

• Journal of Microbiology and Biotechnology
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• v.26 no.5
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• pp.823-828
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• 2016

The present study investigated the protective effect of naturally purified 4-(3,4-dihydroxyphenyl)-3-buten-2-one (DHP) from Phellinus linteus against naproxen-induced gastric antral ulcers in rats. To verify the protective effect of DHP on naproxen-induced gastric antral ulcers, various doses (1, 5, and 10 μg/kg) of DHP were pretreated for 3 days, and then gastric damage was caused by 80 mg/kg naproxen applied for 3 days. DHP prevented naproxen-induced gastric antral ulcers in a dose-dependent manner. In particular, 10 μg/kg DHP showed the best protective effect against naproxen-induced gastric antral ulcers. Moreover, DHP significantly attenuated the naproxen-induced lipid peroxide level in gastric mucosa and increased the activities of radical scavenging enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, in a dose-dependent manner. A histological examination clearly demonstrated that the gastric antral ulcer induced by naproxen nearly disappeared after the pretreatment of DHP. These results suggest that DHP can inhibit naproxen-induced gastric antral ulcers through prevention of lipid peroxidation and activation of radical scavenging enzymes.

• Journal of Microbiology and Biotechnology
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• v.21 no.4
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• pp.400-404
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• 2011

Indomethacin is a nonsteroid anti-inflammatory agent that is known to induce severe gastric mucosal lesions. In this study, we investigated the effect of selenium on gastric mucosal lesions in rats. To confirm the curative effect of selenium against indomethacin-induced gastric ulcers, gastric ulcers were induced by oral administration of 25 mg/kg indomethacin, and then different doses (10, 50, and 100 ${\mu}g$/kg of body weight) of selenium or vehicle were treated by oral gavage for 3 days. Oral administration of indomethacin clearly increased the gastric ulcer area in the stomach, whereas selenium applied for 3 days significantly decreased the gastric ulcer area in a dose-dependent manner. In addition, selenium markedly reduced the increase of lipid peroxidation induced by indomethacin in the gastric mucosa and increased activities of radical scavenging enzymes such as superoxide dismutase, catalase, and glutathione peroxidase in a dose-dependent manner. These results reveal that selenium can heal indomethacin-induced gastric ulcers through elimination of the lipid peroxides and activation of radical scavenging enzymes.

• Environmental Analysis Health and Toxicology
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• v.30
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• pp.6.1-6.7
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• 2015

Objectives This study aimed to estimate the effects of 4-nonylphenol (NP), a ubiquitously present surfactant in aquatic environments, on the anti-oxidant systems of the liver in the Far Eastern catfish Silurus asotus. Methods Changes in biochemical parameters involved in glutathione (GSH)-related and other anti-oxidant systems were analyzed following 4 weeks of 4-NP administration (0.1 and 1.0 mg/kg diet) via a formulated diet to catfish. Results 4-NP exposure induced an elevation in hepatic lipid peroxide levels and an accompanying decrease in reduced state GSH after 2 weeks, suggesting pro-oxidant effects of the chemical in catfish. This oxidative stress was associated with an inhibition of the GSH-utilizing enzyme glutathione peroxidase at the same time point. This inhibition was restored after 4 weeks. The activities of other anti-oxidant enzymes, i.e., glutathione reductase, superoxide dismutase and catalase were increased after 4 weeks. These enzyme increases occurred more strongly at the higher 4-NP concentration (1.0 mg/kg diet). Conclusions 4-NP given to catfish at 0.1 to 1.0 mg/kg diet, concentrations relevant to environmental levels, depletes the endogenous anti-oxidant molecule GSH and temporarily inhibits GSH-related anti-oxidant enzymes. Such declines in anti-oxidant capacity and elevated oxidative stress seem to be compensated eventually by subsequent activation of various anti-oxidant enzyme systems.

• International Journal of Industrial Entomology and Biomaterials
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• v.35 no.1
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• pp.39-44
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• 2017

The venome of Phoneutria nigriventer spider has been shown to have side effects including severe painful erections that last for hours. PnTx2-6, a toxin from P. nigriventer spider venom, modulates voltage gated $Na^+$ channels and activation of nitric oxide (NO) production. NO is essential for the regulation of blood flow and pressure. Therefore, PnTx2-6 is expected to be effective not only for erectile dysfunction but also for cardiovascular diseases. A previously has reported cDNA clone for PnTx2-6 toxin, which was expressed in E. coli cytoplasm. We created the same clone and expressed it in a bacterial expression system. PnTx2-6 increased the genes expression of superoxide dismutase 1, glutathione peroxidase 1, and sulfiredoxin 1. We hypothesized that recombinant PnTx2-6 may indirectly regulate blood flow and pressure, resulting in NO production in human umbilical vein endothelial cells (HUVEC). These data suggest differential regulation of the vascular ageing process, which may contribute to the anatomic heterogeneity of atherosclerosis. The results of this study may be used for the emergency treatment of sudden cardiovascular disease caused by ageing.

• Natural Product Sciences
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• v.9 no.4
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• pp.235-240
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• 2003

Tectorigenin has an apoptosis-inducing ability and immunosuppressive activity. We investigated the effect of tectorigenin on Phase I and II enzyme activities to elucidate the pharmacological action of the immunosuppressive tectorigenin in the diabetic rat. This compound was obtained from the hydrolysis of tetoridin isolated from the flower of Pueraria thumbergiana (Leguminosae). This crude drug (Puerariae Flos) has been used as a therapeutic for diabetes mellitus in traditional Korean medicine. Tecotrigenin inhibited the formation of malondialdehyde (MDA) and hydroxy radicals in serum and liver but promoted superoxide dismutase (SOD) activity. Low MDA contents and low xanthine oxidase and aldehyde oxidase activities were observed in the tectorigenin-treated rats, suggesting that such Phase I enzyme activities are the major source of lipid peroxidation. However, tectorigenin increased Phase II enzyme activities such as SOD, glutathione peroxidase and catalase, suggesting the activation of free radical-scavenging enzymes. The activities of tectorigenin were comparable to those of glibenclamide, which was employed as a positive control. These results suggest that tectorigenin may share some biological properties with glibenclamide in insulin-dependent-diabetes mellitus (IDDM).

• Journal of Korean Biological Nursing Science
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• v.23 no.3
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• pp.247-255
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• 2021

Purpose: The goal of this study was to see how different aerobic exercise intensities affected AMP-activated protein kinase (AMPK), reactive oxygen, and antioxidant enzymes in young mice during an 8-week period. Methods: Forty male C57BL/6 mice, aged seven weeks, were randomly assigned to one of four groups: control (n=10), low-intensity exercise (n=10), moderate-intensity exercise (n=10), and high-intensity exercise (n=10). For eight weeks, aerobic activity was performed once a day for 35-40 minutes, five days a week. The data were analyzed using descriptive statistics, analysis of variance (ANOVA), chi-squared tests, and the Tukey test in the SPSS/WIN 25.0 program. Results: Weight (p=.001) was substantially different between the moderate-intensity exercise group and the control group in AMPK (p<.001). In addition, there were no significant differences between the moderate-intensity exercise group and the control group in reactive oxygen malondialdehyde (MDA) levels (p=.136) and antioxidant enzyme superoxide dismutase (SOD) levels (p=.521). Conclusion: These findings suggest that moderate-intensity aerobic exercise increased AMPK activation and helped young mice shed weight.

• International Journal of Molecular Medicine
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• v.43 no.6
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• pp.2499-2506
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• 2019

Photoaging is a consequence of chronic exposure to ultraviolet (UV) radiation and results in skin damage. In this study, whether tyndallizate of the probiotic bacterium Lactobacillus acidophilus IDCC 3302 (ACT 3302) can protect against UVB-induced photodamage to the skin was investigated. For this, HaCaT keratinocytes were used as a model for skin photoaging. HaCaT cells were treated with ACT 3302 prior to UVB exposure and skin hydration factors and matrix metalloproteinase (MMP)-1, MMP-2, and MMP-9 levels in the culture supernatant were evaluated by ELISA. The protective effects of ACT 3302 against UVB-induced oxidative stress in HaCaT cells was also assessed by measuring superoxide dismutase and catalase activity and detecting the expression of pro-inflammatory cytokine-encoding genes and mitogen-activated protein kinase (MAPK) signaling components by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. UVB exposure increased MMP expression and MAPK activation; these changes were attenuated by pretreatment with ACT 3302. Treatment with ACT 3302 prior to UVB exposure also attenuated inflammation. These results demonstrate that tyndallized ACT 3302 can mitigate photodamage to the skin induced by UVB radiation through the suppression of MMPs and could therefore be used clinically to prevent wrinkle formation.

• Journal of Life Science
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• v.24 no.1
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• pp.20-25
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• 2014

In the present study, the curative effect of curcumin on indomethacin-induced gastric mucosal lesions in rats was investigated. Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID), with serious side effects, including erosion, ulcerative lesions, and petechial bleeding in the mucosa of the stomach. Gastric mucosal lesions were caused by oral administration of 25 mg/kg of indomethacin. Various doses (10, 50, and 100 mg/kg) of curcumin were treated for 3 days by oral gavage. Indomethacin clearly increased the gastric ulcer area in the stomach, and curcumin significantly decreased the gastric ulcer area in a dose-dependent manner. Curcumin also markedly inhibited lipid peroxidation in the gastric mucosa and activated radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, in a dose-dependent manner. These results suggest that curcumin can induce recovery from indomethacin-induced gastric mucosal lesions through inhibition of lipid peroxidation and activation of radical scavenging enzymes, such as SOD, catalase, and glutathione peroxidase. Curcumin appears to be a powerful free radical quencher, and it may offer an attractive strategy for healing gastric mucosal lesions in humans.