• Journal of Radiation Industry
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• v.4 no.3
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• pp.203-207
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• 2010

Radiation-induced late injury to normal tissue is a primary area of radiation biology research. The present study was undertaken to investigate whether the late effect of the ionizing radiation appears as an age-related oxidative status in the brain. Three groups of 4-month old C57BL/6 mice that were exposed to $^{137}Cs$ ${\gamma}-rays$ at a single dose (5 Gy) or fractionated doses ($1Gy{\times}5times$, or $0.2Gy{\times}25times$) at 2 months old were investigated for the oxidative status of their brains with both young (2-month) and old (24-month) mice. A significant (p<0.05) decrease in superoxide dismutase (SOD) activity was observed in old mice brains compared with that of the young mice. malondialdehyde (MDA) content was significantly (p<0.05) increased in the old mice brain. However, any significant difference in SOD activity and MDA contents of the irradiated brain was not observed compared to age-matched control group mice. SOD activity and MDA content were observed within good parameters of brain aging and there were no late effects on the age-related oxidative level in the ${\gamma}-ray$ irradiated mice brains.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.197-205
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• 2006

Objectives: Anti-oxidants are known to prevent neuronal diseases with pathological and physiological changes such as the brain atrophy and cognitive impairment. This study was designed to investigate the protective effects of Korean ginseng on the oxidative stress induced pathologic changes, and develop new animal model for the brain atrophy. Korean ginseng has anti-oxidant, anti-aging, and protective effects on the brain ischemia. Methods : The intracerebroventricular (ICV) hydrogen peroxide ($H_2O_2$) injection into mice was conducted to generate oxidative stress. Results : The ICV $H_2O_2$ (1 M, $5\;{\mu}l$ injection did not induce either convulsion or death in the acute phase. At the end of second week, cognitive impairment and pathologic change of the brain were observed. The massive brain atrophy was found in the $H_2O_2-injected$ mice, especially in the hippocampus and thalamus. Treatment with Korean ginseng showed a protective effect against the brain atrophy. The $H_2O_2$ injected mice revealed cognitive impairment in the passive avoidance test, and Korean ginseng alleviated cognitive impairment. Conclusion : The results indicate that Korean ginseng has a protective effect on the oxidative stress-induced neuronal damages.

• Proceedings of the Korean Society of Postharvest Science and Technology of Agricultural Products Conference
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• 2003.04a
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• pp.109.2-110
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• 2003

The neuroprotective effect of solvent fraction of native edible plant MK-104 in the mice administered with kainate was evaluated using behavioral sign, neuronal injuries and biomarkers of oxidative stress. Mice, ICR male, were administered with the BFME through a gavage for 4 days consecutively, and on the 3rd day, kainate (450 mg/kg) was i.p. administered. The fraction(400 mg/kg) delayed the onset time of neurobehavioral change (p<0.01), reduced the severity of convulsion and lethality (p<0.05), and restored the level of GSH and lipid peroxidation in brain to control value. A similar protective action was also expressed by fraction-I (200 mg/kg), which showed a prominent protection against the neuronal damage in hippocampal CA1 and CA2 regions (p<0.01) caused by kainate injection. of TBARS value. Based on these results, BFME-I is suggested to contain a functional agent to prevent against oxidative stress in the brain of mice.

• Journal of the Korean Society of Tobacco Science
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• v.31 no.1
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• pp.29-38
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• 2009

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.

• Journal of Nutrition and Health
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• v.36 no.6
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• pp.570-576
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• 2003

The remarkable change of phenomenon induced by stress increase energy metabolism that can induce many reactive oxygen species (ROS) production. ROS can peroxidize cellular macromolecules including lipid and protein. The object of this study was to investigate whether stress may induce cellular damage by producing ROS and whether vitamin E, as a strong lipid-soluble antioxidant, can protect cells against reactive oxygen species produced by noise and immobilization stress in SD rats. The stress group increased 5-hydroxyindole aceti acid (5-HIAA) , one of the stress hormone, in brain tissue and free fatty acid in plasma. Vitamin I treatment had no effect on 5-HIAA but free fatty acid contents decreased with a fortified vitamin I diet. Furthermore, the body weight of vitamin I-treated rats increased more than that of the stress group. Lipid peroxidation and protein degradation as an index of oxidative damage in brain tissue decreased with the use of the fortified vitamin I diet supplement. The results suggest that vitamin I supplements have a protective effect against noise and immobilization stress-induced oxidative damage in brain tissue.

• Journal of Nutrition and Health
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• v.34 no.5
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• pp.525-531
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• 2001

The present study investigated the protective effects of green tea against acute ethanol-induced lipid peroxidation and the change of antioxidative enzyme activities in various regions of rat brain : cortex, cerebellum, striatum and hippocampus. The following parameters were examined : malondialdehyde(MDA) levels and activities of superoxide dismutase(SOD), catalase and glutathione peroxidase(GSH-Px). Male Sprague-Dawley rats were given the experimental containing 1% green tea powder or control diet for 4 weeks, and at the end of feeding diet group received acute ethanol(5g/kg body weight) or equicaloric sucrose solution intragastrically. Green tea powder significantly decreased MDA levels in the striatum compared to control-non alcohol treated group to 1% green tea-non alcohol treated group without altering the antioxidative enzyme activities. Green tea resulted in a significant increase in GSH-Px activities in the hippocampus compared to either control-non alcohol treated group(0.043units/mg protein) or 1% green tea-non alcohol treated group(0.071units/mg protein). In conclusion, these results suggest that moderate consumption of green tea leaves can exert protective effects against ethanol-induced oxidative stress in brain regions, by reducing MDA concentrations in the striatum and enhancing GSH-Px activities in the hippocampus. (Korean J Nutrition 34(5) : 525∼531, 2001)

• The Korea Journal of Herbology
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• v.20 no.3
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• pp.75-81
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• 2005

Objectives : In brain disorders such as ischemic stroke, the final outcome depends largely on the duration and the degree of the ischemia as well as the susceptibility of various cell types in the affected brain region. In the present study, the effects of Nodus Nelumbinis Rhizomatis Extract(NNRe) were tested for the anti-oxidative action of rCBF. Methods : Regional cerebral blood flow(rCBF) were determined by LDF methods. LDF allows for real time, noninvasive, continuous recordings of local CBF. The LDF method has been widely used to trace hemodynamic changes in the superficial or the deep brain structures in experimental stroke research. Results : NNRe treatment showed no change on rCBF in methylene blue, ODQ and L-NNA pretreated rats. 120 minutes of MCAO and followed reperfusion, 0.1% concentration of NNR treatment improved the altered cerebral hemodynamics of cerebral ischemic by increasing rCBF. Conclusions : The ischemia/reperfusion induced oxidative stress may have contributed to cerebral damage in rats, and the present study provides clear evidences for the beneficial effect of NNR on ischemia/reperfusion induced brain injury.

• Biomolecules & Therapeutics
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• v.15 no.1
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• pp.58-64
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• 2007

The previous study reported the biological effect of magnetic field exerted by acting on endocrine and anti-oxidant system. The present study aims to study whether ELF-MF (extremely low frequency magnetic field) affects the physiological endocrine systems such as thyroid and whether ELF-MF affects the defense system against oxidative stress when it alters the function of thyroid. Finally, we correlate the effects of MF on oxidative stress, and adrenal and thyroid with an environmental stress factor. We exposed sham or MF to rats for 5 or 25 days. After the exposure, we determined pain sensitivity, level of TSH, $T_3$ and free $T_4$ in plasma. We also assayed in whole brain, lipid peroxidation, the activity of enzymatic anti-oxidant defense including superoxide dismutase(SOD) and glutathione peroxidase (GPx), and non enzymatic defense such as reduced or oxidized glutathione contents. MF induced the hypersensitivity to thermal stimuli with the reduction of latency. $T_3$ and $T_4$ levels were also increased by the exposure of MF. In addition, we observed the rise of MDA level in rat brain by MF although the MF did not change superoxide dismutase and glutathione peroxidase activity. The effect of MF on both reduced and oxidized glutathione results in decrease in reduced or oxidized glutathione in whole brain. In every experiment, there was no significant difference in MF influence between short term (5 days) and long term (25 days) exposure. Taken together, MF exposure affects the thyroid hormonal control in brain. The elevated thyroid hormone acts on brain, leading to hyper-utilization of oxygen. This phenomenon may be correlated with oxidative stress resulting from MF exposure. In conclusion, we suggest that MF exposure may be an environmental stress by exerting oxidative stress.

• Journal of Sasang Constitutional Medicine
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• v.19 no.3
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• pp.242-256
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• 2007

1. Objectives Purpose of this study is to prove anti-aging and anti-oxidative effects of Gongjinhugwon-dan decoction. 2. Methods The SD rats used in this experiment were 6, 18, and 36 weeks old. Each age group was again divided into three groups. These nine groups consisted of 8 rats each. One group was given no treatment, another group was dosed $200{\mu}l$ of normal saline daily, and the last group was dosed $200{\mu}l$ of 1 % Gongjinhugwon-dan and saline mixture. At the conclusion of the experiment, the age groups were relabelled accordingly (10 weeks, 22 weeks, and 40 weeks). After 4 weeks, change of weight and liver markers were measured. Serum LDL cholesterol, total bilirubin, albumin, glucose, GOT and GPT levels were observed in order to check the hematological modification. Also, each organ tissue was biopsied in order to measure the SOD activity and the glutathione content change. 3. Results & Conclusions Aging did not cause any significant change in GOT and LDH, but GPT and albumin levels showed increase after GHD intake. Serum GPT was lower in the experimental group. Serum total bilirubin of the 40 w GHD group was significantly increased. The populations of dendritic cells in the spleens of the GHD groups were significantly increased. The levels of GSH in the liver of the 40 w GHD group and in the kidney of 22w-GSD were significantly increased in comparison with those of the normal groups. The degenerative change of brain tissue was decreased in the 40 w GHD group compared with those of the 40w normal group and the 40 w saline group. These results suggest that anti-oxidative GSH concentration of liver and kidney in rats treated with GHD showed significant increase in the 40 w GHD group. GHD was effective on increasing anti-oxidative substance in liver and dendritic cells in spleen, thus helping immune system and preventing cell mutation and degenerative change of brain tissues. Further studies and clinical investigation with GHD is needed.

• The Journal of Pediatrics of Korean Medicine
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• v.23 no.3
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• pp.241-262
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• 2009

Objectives This study is designed to investigate the effects of Jujadokseo-hwan on the brain ability and inducing oxidative stresses. Methods We measured the changes of regional cerebral blood flow and mean arterial blood pressure. Then we analyzed histological examination, immunohistochemistric response and anti-oxidant activity of Jujadokseo-hwan. Results 1. Treatment of Jujadokseo-hwan significantly increased regional cerebral blood flow but decreased mean arterial blood pressure. 2. Treatment of Jujadokseo-hwan-induced increase of regional cerebral blood flow was significantly inhibited by pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. 3. In histological examination through TTC stain, group I was no change, but group II showed that discolored in the most cortical part. Group III showed that decreased discolor in the cortical part. 4. In immunohistochemistric response of BDNF, group II showed that lower response effect. Group III showed that increase response effect. 5. Treatment of Jujadokseo-hwan increased proliferation rates of Glial cell effectively 6. Treatment of Jujadokseo-hwan accelerated proliferation rates of C6 cells in vitro. In addition, protective effects on cell death induced by paraquat, rotenone and hydrogen peroxide. In addition, activity of SOD were increased by treatment with Jujadokseo-hwan. Conclusions In conclusion, Jujadokseo-hwan can improve of the brain ability, learning ability, memory ability and induce ischemic brain injuries.