• 공업화학
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• 제29권1호
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• pp.49-55
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• 2018

본 연구에서는 그라비올라의 주성분인 nicotiflorin을 분리하고 그 아글리콘 성분인 kaempferol을 얻어 세포 보호 효과 및 그 보호 메커니즘을 규명하였다. L-Ascorbic acid 및 (+)-${\alpha}$-tocopherol을 대조군으로 하여, $^1O_2$로 유도된 세포 손상에 대해 nicotiflorin 및 kaempferol의 보호 효과를 측정한 결과 nicotiflorin < (+)-${\alpha}$-tocopherol < kaempferol 순으로 보호 효과가 증가하였다. L-Ascorbic acid는 세포 보호 효과를 보이지 않았다. 이들의 세포 보호 효과 메커니즘을 밝히기 위해 singlet oxygen 소광 속도 상수, 자유라디칼 소거 활성, ROS 소거 활성 및 적혈구 세포 침투율을 측정하였다. 실험 결과, kaempferol과 그 배당체인 nicotiflorin의 세포 보호 효과에 있어서 큰 차이는 세포막에의 침투가 가장 큰 요인으로 확인되었다. 대조군 L-ascorbic acid가 항산화능은 크지만 실험 조건에서 세포막에 침투가 잘 안되어 세포 보호 효과가 나타나지 않은 것으로 확인되었다. Kaempferol과 (+)-${\alpha}$-tocopherol의 비교를 통해 세포 침투뿐만 아니라 라디칼 소거활성 및 ROS 소거 활성도 세포 보호 효과에 기여하는 것으로 나타났다. 결론적으로, 광증감 반응으로 유도된 세포막 파괴에 대한 보호작용은 항산화제들의 세포 침투, 자유라디칼 및 ROS 소거 활성이 큰 영향을 미치는 것으로 확인되었다.

• 대한한의학회지
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• 제23권4호
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• pp.113-124
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• 2002

Objects: This research was conducted to investigate the protective effect of Bupleuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils, Methods: To observe the protective effect of Bupleuri Radixon ischemic damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Bupleuri Radix during ischemic damage. Gerbils were divided into three groups: a normal group, a 5-minute two-vessel occlusion (2VO) group and a Bupleun Radix administered group after 2VO. The CCAs were occluded by microclip for 5 minutes, Bupleuri Radix was administered orally for 7 days after 2VO. Histological analysis was performed on the 7th day. For histological analysis, the brain tissue was stained with 1 % of cresyl violet solution. Results: 1. Bupleuri Radix has a protective effect against ischemia in the CA1 area of the gerbil's hippocampus 7 days after 5-minute occlusion. 2. In the hypoxia/reperfusion model using PC12 cells, the Bupleuri Radix has a protective effect against ischemia in the dose of 0.2{\;}\mu\textrm{g}/ml,2{\;}\mu\textrm{g}/ml{\;}and{\;} 20{\;}\mu\textrm{g}/ml$. 3. Bupleuri Radix increased the activities of glutathione peroxidase and catalase. 4. The increased activity of superoxidedismutase (SOD) by ischemic damage might have been induced as an act of self-protection. This study suggests that Bupleuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils. Bupleuri Radix also has protective effect on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions: Bupleuri Radix has protective effect against ischemic brain damage during the early stages of ischemia.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.94.1-94.1
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• 2003

This research was performed to investigate the protective effect of Chungpesagan-tang (CPS) against ischemic damage in PC12 cells. To elucidate the mechanism of the protective effect of CPS on ischemic insult, cell viability and changes in activities of Superoxide dismutase, Glutathione Peroxidase, Catalase, Caspase 3 and the production of Malondialdehyde were observed after treating PC12 cells with CPS which was metabolized by rat liver homogenate. Pretreatment of CPS with liver homogenate increased its protective effect against ischemic insult by reducing the harmful effect of CPS itself. (omitted)

• 대한임상검사과학회지
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• 제46권2호
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• pp.75-78
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• 2014

Green tea and tea polyphenols have been studied extensively as cancer chemopreventive agents in recent years. Epigallocatechin-3-gallate (EGCG) is widely recognized as a powerful antioxidant and a free radical scavenger. The purpose of this study was to evaluate the protective effects of green tea catechins (GTC) on the Bleomycin- and Cyclophosphamide-induced cytotoxicity. Cell viability was measured by MTT assay. In the protective effect of GTC, the cell viability was significantly increased by the treatment of GTC. Furthermore, GTC showed the higher protective effect than EGCG and vitamin E. These results suggest that GTC has the protective effect which is related to the prevention of cancer. Our studies show that the continuous presence of EGCG can reduce radical-induced DNA damage in Chinese hamster lung fibroblast cells (CHL cells).

• 대한한의학회지
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• 제23권3호
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• pp.174-187
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• 2002

Objectives : This study was carried out to determine whether Kamihaengche-tang plus Yulanijihwang-tang (KCYH) exerts a protective effect against oxidant-induced liver cell injury. Methods : Cell injury was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. Results : Oxidants (tBHP and $H_2O_2$) increased dose-dependently LDH release which was significantly prevented by 1% KCYH. The protective effect of KCYH against oxidant-induced cell injury was dose-dependent in the range of 0.05-1 % concentrations. Similarly, KCYH inhibited oxidant-induced lipid peroxidation in a dose-dependent manner. When liver tissues were exposed to Hg (0.5 mM), ALT activity in the medium and lipid peroxidation in tissues were markedly increased. These changes were prevented by 1% KCYH, KCYH restored toxicant-induced inhibition of cellular GSH content. KCYH increased the activities of catalase and glutathion peroxidase in oxidant-treated tissues. Conclusions : These results indicate that KCYH exerts a protective effect against oxidant-induced liver cell injury, and this effect is attributed to prevention of lipid peroxidation. These effects may be due to an increase in concentration of endogenous antioxidants.

• 대한의생명과학회지
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• 제10권4호
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• pp.341-346
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• 2004

Tumor necrosis factor-α (TNF-α) or its mRNA expression are increased in acute nephrosis of various types including ischemia/reperfusion injury. This study was undertaken to determine whether pentoxifylline (PTX), an inhibitor of TNF-α production, provides a protective effect against hypoxia-induced cell injury in rabbit renal cortical slices. To induce hypoxia-induced cell injury, renal cortical slices were exposed to 100% N₂ atmosphere. Control slices were exposed to 100% O₂ atmosphere. The cell injury was estimated by measuring lactate dehydrogenase (LDH) release and p-aminohippurate (PAH) uptake. Exposure of slices to hypoxia increased the LDH release in a time-dependent manner. However, when slices were exposed to hypoxia in the presence of PTX, the LDH release was decreased. The protective effect of PTX was dose-dependent over the concentrations of 0.05∼1 mM. Hypoxia did not increase lipid peroxidation, whereas an organic hydroperoxide t-butylhydroperoxide (tBHP) resulted in a significant increase in lipid peroxidation. PTX did not affect tBHP-induced lipid peroxidation. Hypoxia decreased PAH uptake, which was significantly attenuated by PTX and glycine. tBHP-induced inhibition of PAH uptake was not altered by PTX, although it was prevented by antioxidant deferoxarnine. The PAH uptake by slices in rabbits with ischemic acute renal failure was prevented by PTX pretreatment. These results suggest that PTX may exert a protective effect against hypoxia-induced cell injury and its effect may due to inhibition of the TNF-α production, but not by its antioxidant action.

• 대한본초학회지
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• 제20권2호
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• pp.115-125
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• 2005

Objectives : Polygalae Radix (PR) from Polygalae tenuifolia (Polygalaceae) has been clinically used as a sedative, anti-inflammatory, and anti-bacterial agent. To extend pharmacological effects of PR in the central nervous system (CNS) on the basis of its CNS protective effect, the present study was conducted to identify the effect of PR, whether it shows the neuroprotective action against excitatory neurotoxicity. Methods : To identify the protective effect of PR to excitatory neuro-toxic agent, the present study was focused on the PR effect on cell death, that was caused by applying NMDA to nerve cell, elevation of $(Ca^{2+})_i$, releasement of glutamate, and ROS generation. Result : 1. PR methanol extract, at the concentration range of 0.05 to 5 g/ml, significantly inhibited NMDA (1 mM)-induced neuronal cell death as well as MK-801 (non competitive NMDA antagonist). 2. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited NMDA (1 mM)-induced elevation of cytosolic calcium concentration $[Ca^{2+}]_i$. NMDA application in the presence of MK-801 $(10\;{\mu}M)$ failed to produce the increase of $[Ca^{2+}]_i$ through all the measurement time. 3. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited the NMDA-induced elevation of glutamate release. Also, MK-801 showed similar protective effects. 4. PR methanol extract $(0.5\;{\mu}g/ml)$ inhibited the NMDA-induced elevation of ROS generation. Also, MK-801 showed similar protective effects. Conclusion : The present study provides the availability of PR to exert its protective effect on the neuronal cell death in various neurodegenerative pathophysiological conditions.

• 대한한의학회지
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• 제24권1호
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• pp.29-40
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• 2003

Object : This research was performed to investigate the protective effect of Aurantii Immaturus Fructus against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Aurantii Immaturus Fructus on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Aurantii Immaturus Fructus during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Aurantii Immaturus Fructus administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Aurantii Immaturus Fructus was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after the surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : The results showed that 1. Aurantii Immaturus Fructus had a protective effect against ischemia in the CAI area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, the Aurantii Immaturus Fructus had a protective effect against ischemia in the dose of $0.2{\;}\mu\textrm{g}/ml,{\;}2{\;}\mu\textrm{g}/ml{\;}and{\;}20{\;}\mu\textrm{g}/ml$ 3. Aurantii Immaturus Fructus increased the activities of glutathione peroxidase and catalase, 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Aurantii Immaturus Fructus has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PCq2 cells. Conclusions : Aurantii Immaturus Fructus has protective effects against ischemic brain damage at the early stage of ischemia.

• 대한한의학회지
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• 제24권1호
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• pp.110-121
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• 2003

Objective : This research was performed to investigate the protective effect of Angelicae Dahuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils. Methods : To observe the protective effect of Angelicae Dahuri Radix on ischemia damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Angelicae Dahuri Radix during ischemic insult. Gerbils were divided into three groups : a normal group, a 5-min two-vessel occlusion (2VO) group, and an Angelicae Dahuri Radix administered after 2VO group. The CCAs were occluded by microclip for 5 minutes. Angelicae Dahuri Radix was administered orally for 7 days after 2VO. The histological analysis was performed at 7 days after surgery. For histological analysis, the brain tissue was stained with 1% cresyl violet solution. Results : 1. Angelicae Dahuri Radix has a protective effect against ischemia in the CA1 area of the gerbil hippocampus 7 days after 5-minute occlusion, 2. In the hypoxia/reperfusion model using PC12 cells, Angelicae Dahuri Radix has a protective effect against ischemia in the dose of $0.2\mu\textrm{g}/ml$, $2\mu\textrm{g}/ml$ and $20\mu\textrm{g}/ml$, 3. Angelicae Dahuri Radix increased the activities of glutathione peroxidase and catalase. 4. The activity of superoxide dismutase (SOD) was increased by ischemic damage, which might represent self protection. This study suggests that Angelicae Dahuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils, and it also has protective effects on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions : Angelicae Dahuri Radix has protective effects against ischemic brain damage at the early stage of ischemia.

• 대한의생명과학회지
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• 제7권3호
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• pp.127-131
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• 2001

This study was undertaken to examine the effect of amino acids on anoxia-induced cell injury in rabbit renal cortical slices. In order to induce anoxic cell injury, slices were exposed to a 100% $N_2$ atmosphere and control slices were exposed to 100% $O^2$. Irreversible cell injury was estimated by measuring lactate dehydrogenase (LDH) release and alterations in renal cell function were examined by measuring p-aminohippurate (PAH) uptake. Anoxia caused the increase in LDH release in a time-dependent manner. Glycine and glutathione almost completely prevented anoxia-induced LDH release. Of amino acids tested, glycine and alanine exerted the protective effect against anoxia-induced cell injury. However, asparagine with amide side chain, leucine and valine with hydrocarbon side chain, and basic amino acids (lysine, histidine, and arginine) were not effective. Anoxia-induced inhibition of PAM uptake was prevented by glycine. ATP content was decreased by anoxia, which was not affected by glycine. Anoxia-induced depletion of glutathione was significantly prevented by glycine. These results suggest that neutral amino acids with simple structure exert the Protective effect against anoxia-induced cell injury the involvement of specific interaction of amino acids and cell structure.