• Korean Journal of Food Science and Technology
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• v.46 no.3
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• pp.369-374
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• 2014

The physiological characteristics of kiwi (Actinidia delicosa) fruit were analyzed, which inclued its nutritional composition, in vitro-antioxidant activities, and neuronal cell protective effects. The most abundant components of mineral, amino acid, and fatty acid were found to be potassium (K), glutamic acid, and a-linolenic acid, respectively. The major free sugars were fructose, glucose, and sucrose. In addition, ${\beta}$-carotene and vitamin C contents were $1.35{\mu}g/100mL$ and 29.21 mg/100 g, respectively. The 2,2'-azinobis-(3-ethylbenothiazline-6-sulfonic acid) (ABTS) radical-scavenging activity of the n-hexane fraction obtained from the kiwi extract was 10.52% at a concentration of $1000{\mu}g/mL$. The malondialdehyde (MDA) inhibition of the n-hexane fraction was found to increased in a dose-dependent manner. The intracellular reactive oxygen species (ROS) accumulation after hydrogen peroxide ($H_2O_2$) treatment of PC12 cells was significantly reduced in the presence of the n-hexane fraction compared to PC12 cells treated with $H_2O_2$ only. Moreover, in the a MTT assay, the n-hexane fraction showed in vitro-protective effects against $H_2O_2$-induced neurotoxicity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.11
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• pp.1552-1563
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• 2016

To examine the cognitive function of onion (Allium cepa L.) beverages (odourless and fortified), we analyzed in vitro neuronal cell protection against $H_2O_2$-induced cytotoxicity and performed in vivo tests on amyloid beta ($A{\beta}$)-induced cognitive dysfunction. Cellular oxidative stress and cell viability were evaluated by DCF-DA assay and MTT assay. These results show that fortified beverage resulted in better neuronal cell protection than odourless beverage at lower concentration ($0{\sim}100{\mu}g/mL$). Fortified beverage also showed more excellent acetylcholinesterase (AChE) inhibitory activity ($IC_{50}$: 4.20 mg/mL) than odourless beverage. The cognitive functions of odourless beverage and fortified beverage in $A{\beta}$-induced neurotoxicity were assessed by Y-maze, passive avoidance, and Morris water maze tests. The results show improved cognitive function in both groups treated with beverages. After in vivo tests, cholinergic activities were determined based on AChE inhibition and acetylcholine levels, and antioxidant activities were measured as SOD, oxidized glutathione (GSH)/total GSH ratio, and MDA levels in mouse brain tissue. In a Q-TOF UPLC/MS system, main compounds were analyzed as follows: odourless beverage (five types of sugars and three types of phenolics) and fortified beverages (six types of phenolics and two types of steroidal saponins).

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1111-1119
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• 2004

In this study, we investigated that the effects of corynoxeine on the apoptosis by inducible CT105 in PC 12 cells and neuronpathogenic agent as CT105 confirmed with apoptosis, DNA fragmentation, neurite outgrowth and immunocytochemistry analysis This study examines whether corynoxeine have an anti-alzhmeimer agent by inhibition of apoptosis by CT105 and induces neurite outgrowth. Cytotoxicity was assessed in PC12 cell cultures by DNA fragmentation and measuring lactate dehydrogenase (LDH) in the culture media. The treatment of corynoxeine in exposure of cultures to CT105 and provided complete protection against cytotoxicity. CT105-induced cytotoxicity was blocked by apoptotsis, repaired by DNA fragmentation, neurite outgrowth and exposure to CT105 expression and regenerated with neurite outgrowth and immunocytochemistry by corynoxeine. These results indicate that in neuronal cell cultures, damage of T105, repaired excitotoxicity by corynoxeine and CT105-induced cytotoxicity is blocked primarily by the activation of anti-apoptosis.

• Natural Product Sciences
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• v.16 no.2
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• pp.99-106
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• 2010

This experiment was undertaken to investigate whether methanol extract of fruit peel of Dimocarpus longan Lour. (MEFL) protects against kainic acid (KA)-induced seizure. Oral administration of MEFL (1, 2 and 4 mg/kg) increased KA (50 mg/kg)-induced survival rate and latency of convulsion onset, and deceased seizure scores and weight loss induced by intraperitoneal (i.p) injection of KA in mice. In addition, MEFL protected against cell death in the hippocampus of rat brain after KA-administration as analyzed by using TUNEL assay in rats. MEFL also significantly blocked seizure-form of electroencephalogram (EEG) power spectra induced by KA in rats. MEFL also inhibited elevation of [$Ca^{2+}$]i and increased [$Cl^-$]i induced by KA in cultured neuronal cells. Therefore, it is suggested that MEFL protects against seizure induced by KA, decreasing [$Ca^{2+}$]i.

• BMB Reports
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• v.54 no.9
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• pp.458-463
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• 2021

Cytokines activate inflammatory signals and are major mediators in progressive β-cell damage, which leads to type 1 diabetes mellitus. We recently showed that the cell-permeable Tat-CIAPIN1 fusion protein inhibits neuronal cell death induced by oxidative stress. However, how the Tat-CIAPIN1 protein affects cytokine-induced β-cell damage has not been investigated yet. Thus, we assessed whether the Tat-CIAPIN1 protein can protect RINm5F β-cells against cytokine-induced cytotoxicity. In cytokine-exposed RINm5F β-cells, the transduced Tat-CIAPIN1 protein elevated cell survivals and reduced reactive oxygen species (ROS) and DNA fragmentation levels. The Tat-CIAPIN1 protein reduced mitogen-activated protein kinases (MAPKs) and NF-κB activation levels and elevated Bcl-2 protein, whereas Bax and cleaved Caspase-3 proteins were decreased by this fusion protein. Thus, the protection of RINm5F β-cells by the Tat-CIAPIN1 protein against cytokine-induced cytotoxicity can suggest that the Tat-CIAPIN1 protein might be used as a therapeutic inhibitor against RINm5F β-cell damage.

• YAKHAK HOEJI
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• v.60 no.2
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• pp.92-99
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• 2016

Parkinson's disease (PD) is one of the representative neurodegenerative movement disorders with the selective loss of dopaminergic neurons in the substantia nigra. 6-Hydroxydopamine (6-OHDA) is widely used as an experimental model system to mimic PD and has been reported to cause neuronal cell death via oxidative and/or nitrosative stress. Therefore, daily intake of dietary or medicinal plants which fortifies cellular antioxidant capacity can exert neuroprotective effects in PD. In the present study, we have investigated the protective effect of Korean red ginseng (KRG) against 6-OHDA-induced nitrosative death in C6 glioma cells. Treatment of C6 cells with 6-OHDA decreased cell viability and increased expression of inducible nitric oxide synthase, production of nitric oxide as well as peroxynitrite, and formation of nitrotyrosine. 6-OHDA led to apoptotic cell death as determined by decreased Bcl-2/Bax, phosphorylation of JNK, activation of caspase-3, and cleavage of PARP. Conversely, pretreatment of C6 cells with KRG attenuated 6-ODHA-induced cytotoxicity, apoptosis, and nitrosative damages. To further elucidate the molecular mechanism of KRG protection against 6-OHDA-induced nitrosative cell death, we have focused on the cellular self-defense molecules against exogenous noxious stimuli. KRG treatment up-regulated heme oxygenase-1 (HO-1), a key antioxidant enzyme essential for cellular defense against oxidative and/or nitrosative stress via activation of Nrf2. Taken together, these findings suggest KRG may have preventive and/or therapeutic potentials for the management of PD.

• BMB Reports
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• v.49 no.11
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• pp.617-622
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• 2016

Oxidative stress is closely associated with various diseases and is considered to be a major factor in ischemia. NAD(P)H: quinone oxidoreductase 1 (NQO1) protein is a known antioxidant protein that plays a protective role in various cells against oxidative stress. We therefore investigated the effects of cell permeable Tat-NQO1 protein on hippocampal HT-22 cells, and in an animal ischemia model. The Tat-NQO1 protein transduced into HT-22 cells, and significantly inhibited against hydrogen peroxide ($H_2O_2$)-induced cell death and cellular toxicities. Tat-NQO1 protein inhibited the Akt and mitogen activated protein kinases (MAPK) activation as well as caspase-3 expression levels, in $H_2O_2$ exposed HT-22 cells. Moreover, Tat-NQO1 protein transduced into the CA1 region of the hippocampus of the animal brain and drastically protected against ischemic injury. Our results indicate that Tat-NQO1 protein exerts protection against neuronal cell death induced by oxidative stress, suggesting that Tat-NQO1 protein may potentially provide a therapeutic agent for neuronal diseases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.6
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• pp.1433-1440
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• 2003

This research was performed to investigate protective effect of Sophorae subprostratae Radix and each fractions against ischemic damage using PC12 cells. To observe the protective effect of Sophorae subprostratae Radix on ischemia damage, vibility and changes in activities of Superoxide dismutase (SOD), Glutathione Peroxidase (GPx), Catalase and Production of Malondialdehyde (MDA) were observed after treating PC12 cells with Sophorae subprostratae Radix during ischemic insult. Groups were divided into five groups: no treated (Normal), hypoxia chamber for 48hrs followed by 6h at normoxic chamber (H/R), Sop horae subprostratae Radix total phase treated group with H/R (Total), Sophorae subprostratae Radix water phase treated group with H/R (Water), Sophorae subprostratae Radix BuOH phase treated group with H/R (BuOH), Sophorae subprostratae Radix alkaloid phase treated group with H/R (Alkaloid). The results showed that (1) in hypoxiajreperfusion model using PC12 cell, the Sophorae subprostratae Radix has the protective effect against ischemia in the dose of 0.2 ㎍/㎖, 2 ㎍/㎖ and 20 ㎍/㎖, (2) Sophorae subprostratae Radix increased the activities of glutathione peroxidase and catalase. (3) the activity of Superoxide Diamutase(SOD) increased by ischemic damage, which might represent the self protection. This study suggests that Sophorae subprostratae Radix has neuroprotective effect against neuronal damage following hypoxiajreperfusion cell culture model using PC12 cell and dose dependency effects. In conclusion, Sophorae subprostratae Radix has protective effects against ischemic oxidative damage at the early stage of ischemia.

• The Journal of Korean Medicine
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• v.24 no.1
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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.

• The Journal of Korean Medicine
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• v.24 no.1
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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.