• Preventive Nutrition and Food Science
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• v.13 no.4
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• pp.259-265
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• 2008

This study was designed to investigate the protective effect of fucoidan against AAPH-induced oxidative stress in LLC-PK1 cells (porcine kidney epithelial cells). Oxidative stress was induced by exposing of LLC-PK1 cells to the 1 mM 2,2'-azobis(2-amidino propane) dihydrochloride (AAPH) for 24 hr. Exposure of LLC-PK1 cells to 1 mM AAPH for 24 hr resulted in a significant (p<0.05) decrease in cell viability, but fucoidan treatment protected LLC-PK1 cells from AAPH-induced cell damage in a dose dependant manner. To investigate the protective action of fucoidan against AAPH-induced damage of LLC-PK1 cells, we measured the effects of fucoidan on lipid peroxidation and antioxidant enzymes activities of AAPH treated cells as well as scavenging activities on superoxide anion radical and hydroxyl radical. Fucoidan had protective effect against the AAPH-induced LLC-PK1 cellular damage and decreased lipid peroxidation and increased activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). Furthermore, fucoidan showed strong scavenging activity against superoxide anion radical. The $IC_{50}$ value of fucoidan was $48.37{\pm}1.54\;{\mu}g/mL$ for superoxide anion radical scavenging activity. The fucoidan also had high hydroxyl radical scavenging activity ($IC_{50}=32.03\;{\mu}g/mL$). These results indicate that fucoidan protects against AAPH-induced LLC-PK1 cell damage by inhibiting lipid peroxidation, increasing antioxidant enzyme activities and scavenging offree radicals.

• Korean Journal of Pharmacognosy
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• v.46 no.2
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• pp.109-115
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• 2015

This study was investigated the radical scavenging effect and the protective activity of caffeic acid (CA) against oxidative stress. CA showed strong 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and hydroxyl radical ( OH) scavenging activity, showing 42.00% and 87.22% at 5 μM concentration of DPPH and ·OH scavenging activity, respectively. Furthermore, we studied protective activity of CA from amyloid beta (A${\beta}$_25-35) and lipopolysaccharide (LPS) induced neuronal cell damage and neuronal inflammation using C6 glial cells. The treatment of A${\beta}$_25-35 to C6 glial cell showed declines in cell viability and high generation levels of reactive oxygen species (ROS). However, the treatment of CA increased cell viability. The treatment of 5 ${{\mu}M}$ CA led to the elevation of cell viability from 59.28% to 81.22%. In addition, the production of ROS decreased cellular levels of ROS by the treatment of CA. The treatment of LPS to C6 glial cells increased significant elevation of nitric oxide (NO) production, while CA decreased NO production significantly. The production of NO increased by the treatment of LPS to 131.08%, while CA at the concentration of 1 ${{\mu}M}$ declined the NO production to 104.86%. The present study indicated thatCA attenuated A${\beta}$_25-35-induced neuronal oxidative stress and inflammation by LPS, suggesting as a promising agent for the neurodegenerative diseases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1459-1466
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• 2006

The water extract of Hwansodan has been traditionally used for treatment of ischemic brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of Hwansodan rescues cells from neurodegenerative disease. PC12 pheochromocytoma cells have been used extensively as a model for studying the cellular and molecular mechanisms of neuronal cell damages. Under deprivation of growth factor and ischemic injury, PC12 cells spontaneously undergoes apoptotic cell death. Serum and glucose deprivation markedly decreased the viability of PC12 cells, which was characterized with apparent apoptotic features such as membrane blebbing as well as fragmentation of genomic DNA and nuclei. However, the aqueous extract of Hwansodan significantly reduced serum and glucose deprivation-induced cell death and apoptotic characteristics through reduction of intracellular peroxide generation. Pretreatment of Hwansodan also ingibited the activation of caspase-3, in turn, degradation of ICAD/DFF45 was completely abolished in serum and glucose deprivated cells. Furthermore, pretreatment of Hwansodan obviously increased heme oxygenase 1 (HO-1) expression in PC12 cells. Taken together, the data suggest that the protective effects of Hwansodan against serum and glucose deprivation induced oxidative injuries may be achieved through the scavenging of reactive oxygene species accompanying with HO-1 induction.

• Journal of Korean Neurosurgical Society
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• v.38 no.6
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• pp.456-464
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• 2005

Objective : The authors investigated whether rotenone induces cellular death also in non-dopaminergic neurons and high concentration of potassium ion can show protective effect for non-dopaminergic neuron in case of rotenone-induced cytotoxicity. Methods : Neuro 2A cells was treated with rotenone, and their survival as well as cell death mechanism was estimated using 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium[MTT] assay, Lactate dehydrogenase[LDH] release assay, fluorescence microscopy, and agarose gel electrophoresis. The changes in rotenone-treated cells was also studied after co-treatment of 50mM KCl. And the protective effect of KCl was evaluated by mitochondrial membrane potential assay and compared with the effects of various antioxidants. Results : Neuro 2A cells treated with rotenone underwent apoptotic death showing chromosome condensation and fragmentation as well as DNA laddering. Co-incubation of neuro 2A cells with 50mM KCl prevented it from the cytotoxicity induced by rotenone. Intracellular accumulation of reactive oxygen species[ROS] resulting by rotenone were significantly reduced by 50mM KCl. Potassium exhibited significantly similar potency compared to the antioxidants. Conclusion : The present findings showed that potassium attenuated rotenone-induced cytotoxicity, intracellular accumulation of ROS, and fragmentation of DNA in Neuro 2A cells. These findings suggest the therapeutic potential of potassium ion in neuronal apoptosis, but the practical application of high concentration of potassium ion remains to be settled.

• Journal of the Korean Applied Science and Technology
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• v.27 no.4
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• pp.559-567
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• 2010

In this study, the antioxidative effect, cellular protective effect and inhibitory effect on tyrosinase of Cosmos bipinnatus extracts were investigated. The ethyl acetate fraction of Cosmos bipinnatus flower extract ($11.48\;{\mu}g$/mL) showed more excellent free radical (1,1-diphenyl-2-picrylhydrazyl radical, DPPH) scavenging activity (FSC50) than those of leaf and stem extracts ($17.45\;{\mu}g$/mL). Reactive oxygen species (ROS) scavenging activity (OSC50) of Cosmos bipinnatus extracts on ROS generated in $Fe^{3+}$-EDTA/H2O2 system were investigated using the luminol-dependent chemiluminescence assay. The ethyl acetate fraction of Cosmos bipinnatus flower extract ($0.56\;{\mu}g$/mL) showed 3 times more excellent ROS scavenging activity than L-ascorbic acid ($1.50\;{\mu}g$/mL). The protective effects of the ethyl acetate fractions of extracts from different parts of Cosmos bipinnatus on the rose-bengal sensitized photohemolysis of human erythrocytes were investigated. The ethyl acetate fractions of leaf and stem extract and flower extracts suppressed photohemolysis in a concentration dependent manner ($10\sim50\;{\mu}g$/mL). The inhibitory effect of ethyl acetate fraction of Cosmos bipinnatus flower extract ($62.75\;{\mu}g$/mL) on tyrosinase was investigated to assess the whitening efficacy. The ethyl acetate fraction of Cosmos bipinnatus flower extract showed 3.5 times higher tyrosinase inhibitory effect than arbutin ($226.88\;{\mu}g$/mL) known as an effective whitening agent. These results indicate that fractions of Cosmos bipinnatus extracts can function as antioxidants in biological systems, particularly skin exposed to UV radiation by scavenging $^1O2$ and other ROS, and protect cellular membranes against ROS. Fractions of Cosmos bipinnatus extracts can be applicable to new functional cosmetics for antioxidant and whitening.

• Preventive Nutrition and Food Science
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• v.21 no.3
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• pp.208-220
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• 2016

The aim of this study was to investigate the protective effects of juice powders from sweet orange [Citrus sinensis (L.) Osbeck], unshiu mikan (Citrus unshiu Marcow), and mini tomato (Solanum lycopersicum L.), and their major flavonoids, hesperidin, narirutin, and rutin in tert-butyl hydroperoxide (t-BHP)-induced oxidative stress in HepG2 cells. The increased reactive oxygen species and decreased glutathione levels observed in t-BHP-treated HepG2 cells were ameliorated by pretreatment with juice powders, indicating that the hepatoprotective effects of juice powders and their major flavonoids are mediated by induction of cellular defense against oxidative stress. Moreover, pretreatment with juice powders up-regulated phase-II genes such as heme oxygenase-1 (HO-1), thereby preventing cellular damage and the resultant increase in HO-1 expression. The high-performance liquid chromatography profiles of the juice powders confirmed that hesperidin, narirutin, and rutin were the key flavonoids present. Our results suggest that these fruit juice powders and their major flavonoids provide a significant cytoprotective effect against oxidative stress, which is most likely due to the flavonoid-related bioactive compounds present, leading to the normal redox status of cells. Therefore, these fruit juice powders could be advantageous as bioactive sources for the prevention of oxidative injury in hepatoma cells.

• Journal of Ginseng Research
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• v.42 no.3
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• pp.389-399
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• 2018

Background: The antioxidant effects of Panax ginseng have been reported in several articles; however, little is known about the antimelanogenesis effect, skin-protective effect, and cellular mechanism of Panax ginseng, especially of P. ginseng calyx. To understand how an ethanol extract of P. ginseng berry calyx (Pg-C-EE) exerts skin-protective effects, we studied its activities in activated melanocytes and reactive oxygen species (ROS)-induced keratinocytes. Methods: To confirm the antimelanogenesis effect of Pg-C-EE, we analyzed melanin synthesis and secretion and messenger RNA and protein expression levels of related genes. Ultraviolet B (UVB) and hydrogen peroxide ($H_2O_2$) were used to induce cell damage by ROS generation. To examine whether this damage is inhibited by Pg-C-EE, we performed cell viability assays and gene expression and transcriptional activation analyses. Results: Pg-C-EE inhibited melanin synthesis and secretion by blocking activator protein 1 regulatory enzymes such as p38, extracellular signal-regulated kinases (ERKs), and cyclic adenosine mono-phosphate response element-binding protein. Pg-C-EE also suppressed ROS generation induced by $H_2O_2$ and UVB. Treatment with Pg-C-EE decreased the expression of matrix metalloproteinases, mitogen-activated protein kinases, and hyaluronidases and increased the cell survival rate. Conclusion: These results suggest that Pg-C-EE may have antimelanogenesis properties and skin-protective properties through regulation of activator protein 1 and cyclic adenosine monophosphate response element-binding protein signaling. Pg-C-EE may be used as a skin-improving agent, with moisture retention and whitening effects.

• Journal of Oriental Neuropsychiatry
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• v.24 no.3
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• pp.309-320
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• 2013

Objectives : There is a possibility LRE as remedy in Alzheimer disease (AD), but it's nerve protection effect and mechanism have to be elucidate. In this research, we applied LRE on $A{\beta}_{25-35}$ pre-treated SH-SY5Y cells, to find out the nerve protection effect and mechanism in AD cell model. Methods : We tried to confirm that effect by experimenting with 20, 50, and $100{\mu}g/ml$ concentration of LRE as a medicine. Next experiment, we assessed damage effect which induced $A{\beta}_{25-35}$, known to cause AD, on SH-SY5Y cell. In addition, cellular viability test is executed under $H_2O_2$ treatment condition in a SH-SY5Y cell. Results : 1. In $A{\beta}_{25-35}$ treated SH-SY5Y cell, LRE exhibited an anti-phosphorylation effect about tau protein, JNK, and IKB. 2. LRE prevent nerve cell apoptosis, which indued $A{\beta}_{25-35}$ and oxidative stress, modify JNK engaged synaptic structure and $NF{\kappa}B$ induced p75-neurotrophin receptor polymorphism. Conclusions : We found that LRE prevented oxidative stress-induced cellular destruction, for example, increased SOD activity of $A{\beta}_{25-35}$ treated SH-SY5Y cell and reduced toxicity of oxygen free radical. Consequently, the ingredients of LRE have a role as a catalyzer for $A{\beta}_{25-35}$ clearance and as scavenger for active oxygen free radical.

• Biomolecules & Therapeutics
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• v.6 no.4
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• pp.371-377
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• 1998

The aim of the present study was to investigate the effect of Palmiwon on the type 1-prediabetic models induced by streptozotocin (STZ) in RINm5F cells and HIT-T15 cells. Palmiwon increased the cell proliferation and insulin release when pre- and post-treated for the STZ-exposed pancreatic beta cells. The cell proliferation and insulin release of these beta cells were measured by $^3$H-thymidine uptake and RIA, respectively. We also analyzed nutrients such as sugars, fatty acid and amino acids and minerals containing in Palmiwon using by gas chromatography, amino acid analyzer and AA spectrometer, respectively. Palmiwon seems to have protective and recovery properties on the prediabetic model in cellular level, which were ascribe to various nutrients and minerals containing in Palmiwon. From these results, it could be suggested that Palmiwon may be available as preventive and therapeutic prescription of type 1 diabetes mellitus.

• YAKHAK HOEJI
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• v.32 no.1
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• pp.70-79
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• 1988

The effect of Ginseng on global myocardial ischemia and reperfusion was examined in isolated perfused rat hearts. The Ginseng ethanol extract (100mg/kg/day) was administered orally for 10 days. The rat hearts were removed and perfused at 75cm $H_{2}O$ by the Langendorff method. After 25 min. of global ischemia, the hearts were reperfused. The myocardial contents of adenosine 5'-triphosphate, creatine phosphate, and calcium were assayed. There no differences in ATP levels in all group of normal and Ginseng-treated hearts. Both in non-ischemic and ischemic heart, Ginseng increased significantly tissue creatine phosphate levels compared with control. Whereas, in ischemic-reperfused heart, there was no significant difference. In the control groups, myocardial calcium contents in the ischemic hearts were decreased compared with the non-ischemic hearts. But, in the Ginseng-treated groups, the calcium contents in the ischemic herts were not changed with the nonischemic hearts. Therefore, Ginseng appears to exert its protective effect against ischemic heart condition, not against ischemic-reperfused heart condition, by regulating energy metabolism and maintaing cellular function.