• The Korea Journal of Herbology
• /
• v.21 no.4
• /
• pp.77-84
• /
• 2006

Objectives : To evaluate the neuroprotective effects of modified Bo-Yang-Hwan-O-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in N2a neuroblastoma cells. Methods : To study the cytotoxic effect of BHT on N2a neuronal cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, N2a neuronal cells were induced oxidative damages by H2O2, and assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effects of BHT by tube test. Results : In MTT assay, $500{\mu}g/ml$ of BHT was not showed cytotoxic effect on N2a neuronal cells. BHT protected N2a neuronal cells from H2O2-induced cell death in a dose-dependent manner. BHT also protected N2a neuronal cells from H2O2-induced DNA fragmentation. BHT scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong anti-oxidant effects through the free radical scavenging and neuroprotective effects in neuronal cells.

• The Korea Journal of Herbology
• /
• v.21 no.4
• /
• pp.85-92
• /
• 2006

Objectives : To evaluate the neuroprotective effects of added Bo-Yang-Hwan-Oh-Tang (BHT), we investigated the neuronal death protection effects to oxidative damages in SH-SY5Y neuronal cells. Methods : To study the cytotoxic effects of BHT on SH-SY5Y cells, the cell viability was determined by MTT assay. To investigate the neuronal death protection of BHT, SH-SY5Y cells were induced oxidative damages by $H_2O_2$ and then assayed the cell viability and DNA fragmentation. We also investigated DPPH free radical scavenging effect of BHT by tube test. Results : In MTT assay, $1000{\mu}g/ml$ of BHT was not showed the cytotoxic effect on SH-SY5Y cells. BHT protected SHSY5Y cells from $H_2O_2-induced $ neuronal cell death in a dose-dependent manner. BHT also protected SH-SY5Y cells from $H_2O_2-induced$ DNA fragmentation. BHT effectively scavenged DPPH free radicals in a dose-dependent manner. Conclusion : These data suggest that BHT may have strong antioxidant effects through the free radical scavenging and neuroprotective effects in human neuronal cells.

• Herbal Formula Science
• /
• v.16 no.2
• /
• pp.193-204
• /
• 2008

Dehydrocostus lactone (DHL) and Mokko lactone (ML) were isolated from Saussureae Radix, and their effects on heme oxygenase-1 (HO-1) expression and hepatoprotection in the liver cell line HepG2 were investigated. DHL induced HO-1 expression and HO activity in a dose-dependent manner, whereas ML lacking one double bond property at 11 and 13 carbons on its own chemical structure had no apparent effects. DHL also induced Nrf2 nuclear translocation and enhanced antioxidant response element (ARE) activation which mediated HO-1 gene transcription. Pretreatment with DHL protected HepG2 cells against oxidative damages caused by H2O2. Interestingly, the hepatoprotective effects of DHL appeared to be associated with HO enzymatic activation, HO-1 expression and Nrf2 activation, because blockage of HO activity by a HO inhibitor and inhibition of HO-1 and Nrf2 cellular synthesis by small interfering RNA abolished heptoprotection afforded by DHL. Taken together, this investigation provides evidence supporting that Saussureae Radix is hepatoprotective against oxidative stress that causes abnormal liver damages.

• Journal of Ginseng Research
• /
• v.39 no.4
• /
• pp.299-303
• /
• 2015

Panax ginseng is a well-known economic medical plant that is widely used in Chinese traditional medicine. This species contains a unique class of natural products-ginsenosides. Recent clinical and experimental studies have presented numerous lines of evidence on the promising role of ginsenosides on different diseases including neurodegenerative diseases, cardiovascular diseases, and certain types of cancer. Nowadays, most of the attention has focused on ginsenoside Rd as a neuroprotective agent to attenuate ischemic stroke damages. Some of the evidence showed that ginsenoside Rd ameliorates ischemic stroke-induced damages through the suppression of oxidative stress and inflammation. Ginsenoside Rd can prolong neural cells' survival through the upregulation of the endogenous antioxidant system, phosphoinositide-3-kinase/AKT and extracellular signal-regulated protein kinase 1/2 pathways, preservation of mitochondrial membrane potential, suppression of the nuclear factor-kappa B, transient receptor potential melastatin, acid sensing ion channels 1a, poly(ADP-ribose) polymerase-1, protein tyrosine kinase activation, as well as reduction of cytochrome c-releasing and apoptosis-inducing factor. In the current work, we review the available reports on the promising role of ginsenoside Rd on ischemic stroke. We also discuss its chemistry, source, and the molecular mechanism underlying this effect.

• Journal of Microbiology and Biotechnology
• /
• v.18 no.2
• /
• pp.270-282
• /
• 2008

The yeast Saccharomyces cerevisiae has defense mechanisms identical to higher eukaryotes. It offers the potential for genome-wide experimental approaches owing to its smaller genome size and the availability of the complete sequence. It therefore represents an ideal eukaryotic model for studying cellular redox control and oxidative stress responses. S. cerevisiae Yap1 is a well-known transcription factor that is required for $H_2O_2$-dependent stress responses. Yap1 is involved in various signaling pathways in an oxidative stress response. The Gpx3 (Orp1/PHGpx3) protein is one of the factors related to these signaling pathways. It plays the role of a transducer that transfers the hydroperoxide signal to Yap1. In this study, using extensive proteomic and bioinformatics analyses, the function of the Gpx3 protein in an adaptive response against oxidative stress was investigated in wild-type, gpx3-deletion mutant, and gpx3-deletion mutant overexpressing Gpx3 protein strains. We identified 30 proteins that are related to the Gpx3-dependent oxidative stress responses and 17 proteins that are changed in a Gpx3-dependent manner regardless of oxidative stress. As expected, $H_2O_2$-responsive Gpx3-dependent proteins include a number of antioxidants related with cell rescue and defense. In addition, they contain a variety of proteins related to energy and carbohydrate metabolism, transcription, and protein fate. Based upon the experimental results, it is suggested that Gpx3-dependent stress adaptive response includes the regulation of genes related to the capacity to detoxify oxidants and repair oxidative stress-induced damages affected by Yap1 as well as metabolism and protein fate independent from Yap1.

• Journal of Haehwa Medicine
• /
• v.20 no.2
• /
• pp.41-52
• /
• 2012

In vitro tests were performed using CST to investigate its role on oxidative damages and inflammatory cytokines. 90% or higher cell viability was observed in CST treated groups from 25 to 200 ${\mu}g/m{\ell}$ using Raw 264.7 cells. CST showed dose-dependent DPPH scavenging activity, with 91.3% and 92.2% scavenging activities at 400 and 800 ${\mu}g/m{\ell}$ concentrations, respectively. CST showed dose-dependent suppression activity of ROS production, especially at 200 ${\mu}g/m{\ell}$ of 41.3%. CST decreased NO production activity, with significant decrease of 16.2% and 33.5% at 100 and 200 ${\mu}g/m{\ell}$ concentrations, respectively. IL-$1{\beta}$, IL-6, MCP-1 production rate were significantly decreased by 30.0%, 27.2%, 22.1% when Raw 264.7 cells were treated with LPS and with CST of 200 ${\mu}g/m{\ell}$. Also, TNF-${\alpha}$ production rate was decreased by 28.6%. The results above indicated therapeutic effect of CST on the AD through anti-oxidative and immune modulatory effect. Various blending of drug substances with CST should be clinically tested.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.35 no.9
• /
• pp.1121-1126
• /
• 2006

In the present study, the potential hepatoprotective effects of poly herbal formulation, Hepa-1000, against oxidative damages induced by t-BHP were evaluated in HepG2 cells in order to relate in vitro antioxidant activity with cytoprotective effects. The t-BHP induced considerable cell damage in HepG2 cells was shown by significant glutamic oxaloacetic transaminase (GOT) and lactate dehydrogenase (LDH) leakage, and increased lipid peroxidation. Hepa-1000-treated cells showed an increased resistance to oxidative challenge, as revealed by higher survival capacity than the one of control cells against t-BHP induced oxidative stress and hepatotoxicity. In addition, the Hepa-1000 had hepatoprotective effects lowering the activity of GOT and LDH, simultaneously. That is, it could inhibit the cell membrane damages resulting in the increased activities of GOT and LDH in the cell culture media. Furthermore, the Hepa-1000 could reduce t-BHP enhanced lipid peroxidation, which was evaluated by measuring the production of malonedialdehyde. Based on the data described above, it could be suggested that the Hepa-1000 has significant hepatoprotective effects and plays a protective role against lipid peroxidation by free radicals.

• Journal of the Society of Cosmetic Scientists of Korea
• /
• v.44 no.4
• /
• pp.375-379
• /
• 2018

In the present study, we have investigated whether methylated marliolide could induce NRF2 thereby exerting anti-oxidant effects. MTT assay showed that methylated marliolide did not exhibit cytotoxicity on HaCaT cells. Methylated marliolide induced a higher ARE-dependent luciferase activation in HaCaT ARE-GFP-luciferase cells, compared with resveratrol. In addition, exposure of methylated marliolide to HaCaT cells significantly induced NRF2 and transcriptionally activated HO-1 and NQO1, both of which are target genes of NRF2. Finally, methylated marliolide protected HaCaT cells against TPA-induced oxidative damages on nucleotides and lipids. Together, results shows that methylated marliolide could suppress oxidative damages through induction of NRF2 which implies that methylated marliolide might serve as a good candidate for novel cosmetic ingredient with anti-oxidant effects.

• Journal of Microbiology and Biotechnology
• /
• v.18 no.8
• /
• pp.1364-1367
• /
• 2008

Oxidative stress damages all cellular constituents, and therefore, cell has to possess various defense mechanisms to cope. Saccharomyces cerevisiae, widely used as a model organism for studying cellular responses to oxidative stress, contains three glutathione peroxidase (Gpx) proteins. Among them, Gpx3 plays a major defense role against oxidative stress in S. cerevisiae. In this study, in order to identity the new interaction proteins of Gpx3, we carried out two-dimensional gel electrophoresis after immunoprecipitation (IP-2DE), and MALDI-TOF mass spectrometry. The results showed that several proteins including protein disulfide isomerase, glutaredoxin 2, and SSY protein 3 specifically interact with Gpx3. These findings led us to suggest the possibility that Gpx3, known as a redox sensor and ROS scavenger, has another functional role by interacting with several proteins with various cellular functions.

• Food Science and Preservation
• /
• v.24 no.4
• /
• pp.536-541
• /
• 2017

Hyperglycemia found in diabetes mellitus causes several physiological abnormalities including the formation of advanced glycation end products (AGEs) and oxidative stress. Accumulation of AGEs and elevation of oxidative stress plays major roles in the development of diabetic complications. Adiponectin secreted from adipocytes is known to improve insulin sensitivity and blood glucose level. Curcumin (CCM), a bioactive component of turmeric, has been reported as a potent antioxidant. Present work aimed to elucidate the roles of CCM in high glucose-induced protein glycation and intracellular events in mature adipocytes. The results demonstrated that CCM inhibited the formation of fluorescent AGEs by approximated 52% at 3 weeks of bovine serum albumin (BSA) glycation with glucose. Correspondingly, CCM decreased the levels of fructosamine and ${\alpha}-dicarbonyl$ compounds during BSA glycation with glucose. These data suggested that CCM might be a new promising anti-glycation agent. Also, CCM reduced high glucose-induced oxidative stress in a dose dependent manner, whereas CCM treatment time-dependently elevated the expression of adiponectin gene in 3T3-L1 adipocytes. The findings from this study suggested the possibility of therapeutic use of CCM for the prevention of diabetic complications and obesity-related diseases.