• Neonatal Medicine
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• v.17 no.2
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• pp.181-192
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• 2010

Purpose: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. Methods: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% $CO_2$ incubators and the other groups were placed in 1% $O_2$ incubators (94% N2, 5% $CO_2$) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% $O_2$). Results: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. Conclusion: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.

• The Journal of Korean Society for Radiation Therapy
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• v.34
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• pp.43-50
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• 2022

Objective: The purpose of this study is to choose a treatment plan and equipment to maximize tangential irradiation to protect the normal brain tissues as much as possible during total scalp irradiation. Subjects and Methods: After zoning the total scalp of a phantom and selecting a target area for treatment, the study made a Helical TomoTherapy(HT) plan, a Helical TomoTherapy with a Complete Block(HTCB) plan, and a Volumetric Modulated Arc Therapy(VMAT) plan. All of these plans made sure that the volume of a treatment plan with 95% of a prescription dose(40 Gy) would not exceed 95% of the entire volume and that Dmax would not be more than 110% of the prescription dose. The therapy plans compared doses among organs at risk of damage including the brain. Doses in the brain tissues were assessed based on the volumetric criteria for normal tissues in Emami et al. Results: HT, HTCB, and VMAT had a dose of 21.68 Gy, 13.75 Gy, and 20.89 Gy, respectively, in brain tissues at D_33%, a dose of 7.06 Gy, 3.21 Gy, and 7.84 Gy, respectively, at D_67%, and a dose of 3.14 Gy, 1.75 Gy, and 3.84 Gy, respectively, at D_100%. They recorded a Dmean of 16.64 Gy, 11.78 Gy, and 16.64 Gy, respectively. These results show that the overall dose was low in the HTCB plan. When the volume of a low dose was calculated based on 5 Gy, they recorded 87%, 49%, and 96%, respectively, in V_5Gy. In addition, the maximum dose in the remaining organ(brain stem, hippocampus, and both lenses) except for the optic pathway was the lowest in HTCB Conclusion: The findings demonstrate that TomoTherapy with a complete block minimized a dose in organs at risk of damage including the brain and hippocampus on both sides and accordingly reduced the probability of side effects such as radiation-induced brain injuries and a resulting decrease in neurocognitive functions. In addition to total scalp irradiation, if additional studies on ring targets treated in various areas are conducted to establish the benefits of tangential irradiation, it is believed that TomoTherapy using Complete Block can be used to maximize tangential irradiation in treatment planning.

• Korean Journal of Food Science and Technology
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• v.38 no.3
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• pp.452-455
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• 2006

The in vitro cytoprotective and anti-oxidative effects of ursodeoxycholic acid, a major active compound from bear's gall were investigated in mouse brain microglia. In the present study, we wished to scrutinize the potential role of UDCA as an anti-neurodegenerative agent in neurodegenerative disease such as Alzheimer's disease. This concept was supported by the multiple preliminary studies in which UDCA has an anti-inflammatory effect in microglial cells. In the study, we found that $7.5\;{\mu}g/mL$ UDCA was effective in the protection of cells from $H_2O_2$ damage, a reactive oxygen, and the resuIt was coincided with the anti-apoptotic effect in DAPI staining. Moreover, the metal-catalyzed oxidation study showed that UDCA has antioxidant effect as much as ascorbic acid at $50{\sim}100\;{\mu}g/mL$. In conclusion, these study results suggested that neuro-degenerative diseases such as Alzheimer's disease probably caused by over-expressed beta amyloid peptide in elderly people can be controled by UDCA through an anti-inflammatory, anti-oxidative and anti-apoptotic effect. The evidences showed in the study may be references for more in-depth in vivo and clinical studies for a candidate of anti-neurodegenerative therapy in the near future.

• Journal of Chest Surgery
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• v.30 no.8
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• pp.752-759
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• 1997

Profound hypothermia protects . cerebral function during total circulatory arrest(TCA) in the surgical treatment of a variety of cardiac and aortic diseases. Despite its importance, there is no ideal technique to monitor the brain injury from ischemia. Since 1994, we have developed compressed spectral array(CSA) of electroencephalography(EEG) and monitored cerebral activity to reduce ischemic injury. The purposes of this study are to analyse the efficacy of CSA and to establish objective criteria to consistently identify the safe level of temperature and arrest time. We studied 6 patients with aortic dissection(AD, n=3) or aortic arch aneurysm(n=3, ruptured in 2). Body temperatures from rectum and esophagus and the EEG were monitored continuously during cooling and rewarming period. TCA with cerebral ischemia was performed in 3 patients and TCA with selective cerebral perfusion was performed in 3 patients. Total ischemic time was 30, 36 and 56 minutes respectively for TCA group and selective perfusion time was 41, 56 and 92 minutes respectively for selective perfusion group. The rectal temperatures for flat EEG were between 16.1 and 22. $1^{\circ}C$ (mean: 18.4 $\pm$ 2.0): the esophageal temperatures between 12.7 and $16.4^{\circ}C$ (mean $14.7\pm1.6).$ The temperatures at which EEG reappeared $5~15.4^{\circ}C$ for esophagus. There was no neurological defic t and no surgical mortality in this series. In summary, the electrical cerebral activity Teappeared within 23 minutes at the temperature less than $16^{\circ}C$ for rectum. It seemed that $15^{\circ}C$ of esophageal temperature was not safe for 20 minutes of TCA and continuous monitoring the EEG with CSA to identify the electrocerebral silence was useful.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.74-84
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• 2002

목적 : 본 실험에서는 gerbil을 이용한 전뇌허혈 동물모델에서 뇌허혈손상 직후 지연성 뇌손상에 대한 대황의 방어효과와 Apoptosis 과정중의 Bax와 Bcl-2 단백질에 대한 조절작용을 관찰하고, TUNEL 염색법을 통하여 대황이 gerbil hippocampus CAl영역의 pyramidal neuron의 세포사에 미치는 영향과 PCl2세포를 이용한 세포배양 모델에서의 대황의 신경방어 효과를 관찰하였다. 방법 : Mongolian gerbil의 총경동맥을 5분간 폐색하여 가역성 전뇌허혈을 유발시킨 후 대황의 전탕액을 하루에 한번 경구 투여하였다. 대황의 신경 보호 효과는 수술 7일 후에 cresyl violet으로 염색하여, 살아있는 신경 세포의 수를 세어 측정하였다. 또, 수술 3일 후에는 면역조직화학적 방범을 통하여 Bax. Bcl-2단백질의 발현과 대황의 신경보호 효과와의 관련성을 알아보았다. 결과： 가역적 전뇌허혈이 일어난 동물군의 경우 hippocampus의 CAl 영역에서 살아있는 신경세포의 수는 $51.0{\pm}2.5개{\;}/mm$에 불과하였으나, 그에 비해 수술 후 7일간 대황을 투여한 동물군은 $106.2{\pm}2.5개{\;}/mm$로 살아 있는 신경세포수가 크게 증가하였다. Apoptosis를 촉진하는 단백질인 Bax의 발현은 3일간 대황을 투여한 동물군의 경우 hippocampus의 CAl 영역에서 현저하게 저해되었고, Apoptosis를 억제하는 Bcl-2 단백질의 발현은 변화가 없었다. TUNEL assay를 통하여 살펴본 결과 대황 투여군의 apoptotic 신경세포사가 감소하였으며 이는 Bax protein의 발현과 유사한 양상을 나타내었다. 결론：대황이 Bax 단백질의 발현을 억제하여 상대적으로 Bax/Bcl-2 자연적 세포사를 억제하여 Mogolian gerbil의 가역성 전뇌허혈 모델에서 신경보호효과를 나타내는 것으로 사료된다.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.50 no.spc1
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• pp.220-223
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• 2005

As functional evaluation of mulberry fruits extracts, the protective effect on cerebral cell and antibacterial activities were carried. $1\%$ HCl-MeOH extract showed $37\%$ cytoprotective effect on hydrogen peroxide, also C3G identified mulberry fruits and cyanidin showed $52\%,\;76\%$, respectively, protective effects on oxygen-glucose deprivation (OGD). In the antibacterial activity of mulberry fruit extracts, MeOB-Cheongil extract showed the highest inhibitory activity. Salmonella typhimurium was shown inhibitory rate more than $70\%$ in all treatment groups. Also Klebsiella pneumoniae was shown inhibitory activity in all treatment groups.

• Korean Journal of Food Science and Technology
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• v.45 no.3
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• pp.350-355
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• 2013

The quality of fermented dropwort extract (FDE) and fermented dropwort vinegar (FDV) was assessed for free sugar, organic acid and free and total amino acid content. Major organic acids were lactic acid in FDE and acetic acid in FDV. Free sugars in FDE were fructose and glucose, and those in FDV were fructose, sucrose, and maltose. Aspartic acid was the major free amino acid in both FDE and FDV. Additionally, the main free amino acids in FDE were alanine and ${\gamma}$-amino-n-butyric acid (GABA), while those in FDV were arginine and valine. Moreover, to investigate the protective effects of FDE and FDV against oxidative stress induced by t-BHP and $H_2O_2$, C6 cells were treated with FDE or FDV prior to inducing the oxidative damage. FDE and FDV inhibited cell death significantly in a dose-dependent manner. These data imply that FDE and FDV may be effective in neuronal cell protection against oxidative damage.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.7
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• pp.886-890
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• 2017

In this study, the protective effect of rice with Phellinus linteus mycelium (PLMR) against hydrogen peroxide-induced oxidative stress was assessed in a mouse hippocampal neuronal HT22 cell line through (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) salt (MTS) assay and western blot. MTS assay using HT22 cells showed that PLMR extract did not affect viability at a concentration range from 1 mg/mL to 5 mg/mL. However, at concentrations over 10 mg/mL, PLMR extract resulted in increased cell death. Cell viability of HT22 was significantly reduced by $H_2O_2$ treatment, and reduction of cell viability was efficiently restored by treatment with PLMR extract in a dose-dependent manner from 0.1 to 1 mg/mL. Cells treated with $H_2O_2$ showed increased expression of Bax, a pro-apoptotic protein, which was down-regulated by treatment with PLMR extract. On the other hand, cells treated with $H_2O_2$ resulted in reduced expression of Bcl-2, an anti-apoptotic protein, which was restored by treatment with PLMR extract. In addition, treatment with PLMR extract reduced expression of cleaved caspase 3 and PARP, which were up-regulated by $H_2O_2$ treatment. The results may suggest that treatment with PLMR extract would suppress $H_2O_2$-induced apoptosis of HT22 cells.

• Journal of agriculture & life science
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• v.46 no.6
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• pp.137-146
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• 2012

This study investigated whether ferulic acid modulates the heme oxygenase (HO)-1 and HO-2 expression in middle cerebral artery occlusion (MCAO)-induced brain injury. Rats (Sprague-Dawley, male) were treated with vehicle or ferulic acid (100 mg/kg, i.v.) before MCAO, and cerebral cortex tissues were collected 24 h after MCAO. This study clearly confirmed the protective effects of ferulic acid during MCAO-induced damage using hematoxylin and eosin staining. MCAO induces nuclear chromatin condensations and necrotic changes with scalloped shrunken form. However, ferulic acid prevented MCAO-induced histopathological changes. HO-1 and HO-2 expression levels were measured using reverse-transcription PCR and Western blot analyses. HO-1 levels were decreased in vehicle-treated animals after MCAO, whereas this decrease in HO-1 levels was attenuated by ferulic acid treatment. However, the level of HO-2 was consistently maintained in the cerebral cortex of vehicle- and ferulic acid-treated animals after MCAO. These results demonstrated that ferulic acid regulates HO-1 expression in ischemic brain injury, while ferulic acid do not modulate HO-2 expression in MACO. In conclusion, these findings suggest that ferulic acid exerts a neuroprotective effect by preventing the MCAO-induced decrease of HO-1 expression.

• Food Science and Preservation
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• v.14 no.2
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• pp.213-219
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• 2007

To develop an anti-dementia agent with potential therapeutic value in the protection of neuronal cells, we selected a water extract of Helianthus annuus seed for analysis. We measured acetylcholinesterase inhibitory activity in the extract, and analyzed the protective effect of the extract on neuronal cell death induced by hydrogen peroxide, or amyloid ${\beta}-peptide$, of SH-SY5Y neuroblastoma cells. The result showed that the extinct exerted protective effects of 83%, 72% and 53% respectively, on cell death induced by 100M, 200M, and 500M hydrogen peroxide. Also, when 50M of amyloid ${\beta}-peptide$ was added to the cells, the extract showed a protective effect (up to 80%) on cell death. Overall, the results showed that the H. annuus extract inhibited acetylcholinesterase activity in a dose-dependent manner, and the extract also strongly protected against cell death induced by hydrogen peroxide or amyloid ${\beta}-peptide$.