• YAKHAK HOEJI
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• v.55 no.5
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• pp.385-390
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• 2011

Bee venom (BV), which is extracted from honeybees, has been used in traditional Korean medical therapy. Glutamate-mediated excitotoxicity contributes to neuronal death in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) or Alzheimer's disease (AD). This study is to investigate the effect of BV on glutamate-induced neurotoxicity on NSC-34 motor neuron cells. To determine the viability of motor neuronal cells, we performed with MTT assays in glutamate-treated NSC-34 cell with BV or without. For the measurement of oxidative stress, DCF assay was used in glutamate-treated NSC-34 motor neuronal cells with BV or without. To investigate the molecular mechanism of BV against glutamate-mediated neurotoxicity in NSC-34 cells, western blot analysis was used. Glutamate significantly decreased cell viability by glutamate dose- or treatment time-dependent manner in NSC-34 cells. However, BV pre-treatment dramatically inhibited glutamate-induced neuronal cell death. Furthermore, we found that BV increased the expression of Bcl-2 protein that is anti-apoptotic protein and reduced the generation of oxidative stress. BV has a neuroprotective role against glutamate neurotoxicity by an increase of anti-apoptotic protein. It suggests that BV may be useful for the reduction of neuronal cell death in neuronal disease models.

• Korean Journal of Pharmacognosy
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• v.48 no.2
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• pp.141-147
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• 2017

As an ongoing study about Allium hookeri (Liliaceae), this study was performed to evaluate the anti-oxidative effect of the leaves of this plant. Ethanol extract of A. hookeri leaves was successively partitioned as methylene chloride, ethyl acetate, n-butanol and $H_2O$ soluble fractions. The ethyl acetate soluble fraction showed the most potent DPPH radical scavenging and superoxide quenching activities among those fractions. To prove antioxidant activity of ethyl acetate fraction of A. hookeri leaves, we checked the activities of superoxide dismutase (SOD) and catalase, and intracellular ROS level and oxidative stress tolerance in Caenorhabditis elegans. In addition, to verify if increased stress tolerance of C. elegans by treating of ethyl acetate fraction was due to regulation of stress-response gene, we checked SOD-3 expression using transgenic strain. As a consequence, the ethyl acetate fraction increased SOD and catalase activity of C. elegans, and reduced intracellular ROS accumulation in a dose-dependent manner. Besides, the ethyl acetate fraction-treated CF1553 worms showed higher SOD-3::GFP intensity.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.3
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• pp.177-187
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• 2021

Metabolic syndrome (MBS) is a widespread disease that has strongly related to unhealthy diet and low physical activity, which initiate more serious conditions such as obesity, cardiovascular diseases and type 2 diabetes mellitus. This study aimed to examine the therapeutic effects of morin, as one of the flavonoids constituents, which widely exists in many herbs and fruits, against some metabolic and hepatic manifestations observed in MBS rats and the feasible related mechanisms. MBS was induced in rats by high fructose diet feeding for 12 weeks. Morin (30 mg/kg) was administered orally to both normal and MBS rats for 4 weeks. Liver tissues were used for determination of liver index, hepatic expression of glucose transporter 2 (GLUT2) as well as both inflammatory and fibrotic markers. The fat/muscle ratio, metabolic parameters, systolic blood pressure, and oxidative stress markers were also determined. Our data confirmed that the administration of morin in fructose diet rats significantly reduced the elevated systolic blood pressure. The altered levels of metabolic parameters such as blood glucose, serum insulin, serum lipid profile, and oxidative stress markers were also reversed approximately to the normal values. In addition, morin treatment decreased liver index, serum liver enzyme activities, and fat/muscle ratio. Furthermore, morin relatively up-regulated GLUT2 expression, however, down-regulated NF-κB, TNF-α, and TGF-β expressions in the hepatic tissues. Here, we revealed that morin has an exquisite effect against metabolic disorders in the experimental model through, at least in part, antioxidant, anti-inflammatory, and anti-fibrotic mechanisms.

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

• The Journal of Internal Korean Medicine
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• v.43 no.4
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• pp.738-750
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• 2022

Objective: Alcohol is known to cause inflammation in the stomach by decreasing the protective substances of the gastric mucosa and increasing oxidative stress. The purpose of this study was to investigate the anti-inflammatory effect of Artemisiae Argyi Folium extract (AF) on alcohol-induced gastritis. Methods: The total polyphenol and flavonoid contents of AF were confirmed through an in vitro experiment. Radical scavenging activities were confirmed using DPPH and ABTS assays. In vivo experiments were conducted on mice divided into 5 groups (n=8): a normal group (Nor), an alcohol-induced gastritis group (Con), an alcohol-induced gastritis group administered 10 mg/kg sucralfate (SC), an alcohol-induced gastritis group administered 100 mg/kg AF (AFL), and an alcohol-induced gastritis group administered 200 mg/kg AF(AFH). The serum levels of reactive oxygen species (ROS) were determined, and protein expressions were confirmed in gastric tissues. Results: In alcohol-induced gastritis, AF alleviated damage to the gastric mucosa caused by alcohol. AF also decreased the serum ROS levels. Western blots showed that AF decreased the expression of NADPH oxidase and decreased the expression of the NF-κB pathway associated with inflammation. AF also decreased the expression of adhesion molecules and chemokine proteins, and increased the expression of anti-inflammatory proteins. Conclusions: AF not only reduced oxidative stress in alcohol-induced gastritis, but it also relieved gastric mucosal inflammation by regulating the expression of the NF-κB pathway.

• The Korea Journal of Herbology
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• v.38 no.1
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• pp.21-30
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• 2023

Objective : Gardeniae Fructus (GF) has bitter and cold nature. Thus, it has been traditionally prescribed in processed form roasted with ginger juice for patients with a weak stomach. This study investigated the effects of processed GF in tert-butyl hydroperoxide (tBHP)-treated gastric epithelial cells. Methods : Processed GF was made by applying 40% ginger juice or 10% ethanol for 24 h and then roasting at 150℃ for 5 minutes. Apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Mitochondrial membrane potential (MMP) was monitored by flow cytometry using the membrane permeable fluorescent dye Rh123. Protein expression was measured by Western blot analysis. Results : Cell viability was reduced by tBHP and restored by ethanol extract of GF (GFE). In the TUNEL assay, it was found that cell death by tBHP was due to apoptosis, and GFE had an anti-apoptotic effect. Processed GF roasted with ginger juice showed the best anti-apoptotic effect. Processed GF also inhibited MMP loss and restored tBHP-induced changes in expression levels of apoptosis-related proteins. Increased ROS production and GSH depletion after tBHP treatment were significantly reduced by processed GF. In addition, tBHP-induced activation of mitogen-activated protein kinase (MAPK) was inhibited by processed GF. Conclusion : These results demonstrate that the processed GF is able to protect gastric epithelial cells from oxidative stress-induced cell death with antiapoptotic and antioxidant activity. In addition, it shows that the processing of GF, which have been traditionally used for gastrointestinal protection, partially have scientific validity.

• Journal of Pharmacopuncture
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• v.27 no.2
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• pp.131-141
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• 2024

Objectives: Polycystic ovary syndrome (PCOS) is one of the most common disorders and it shows up to 20% prevalence in reproductive-aged women populations, but no cures are available to date. We aimed to investigate the protective effects of Changbudodam-tang (CBD) on cell death signaling pathways, inflammation, and oxidative stress observed in Bone-Marrow derived human mesenchymal stem cell (BM-hMSC) by means of PCOS therapeutics in the future. Methods: BM-hMSCs were applied with cell deaths and injuries. Apoptosis and pyroptosis signals were quenched with their related signaling pathways using quantitative PCR, Western blot, and fluorescence image analysis. Results: Our data clearly displayed hydrogen peroxide- and nigericin-treated cell death signaling pathways via regulations of mitochondrial integrity and interleukin (IL)-1β at the cellular levels (p < 0.01 or 0.001). We further observed that pre-treatment with CBD showed protective effects against oxidative stress by enhancement of antioxidant components at the cellular level, with respect to both protein and mRNA expression levels (p < 0.05, 0.01 or 0.001). The mechanisms of CBD were examined by Western blot analysis, and it showed anti-cell death, anti-inflammatory, and antioxidant effects via normalizations of the Jun N-terminal kinase/mitogen-activated protein kinase kinase 7/c-Jun signaling pathways. Conclusion: This study confirmed the pharmacological properties of CBD by regulation of cellular oxidation and the inflammation-provoked cell death condition of BM-hMSCs, which is mediated by the MKK7/JNK/c-Jun signaling pathway.

• The Korea Journal of Herbology
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• v.20 no.3
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• pp.29-41
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• 2005

Objectives : The use of natural products with therapeutic properties is as ancient as human civilisation and, for a long time, mineral, plant and animal products were the main sources of drugs. Catalposide, the major iridoid glycoside isolated from the stem bark of Catalpa ovata G. Don (Bignoniceae) has been shown to possess anti-microbial and anti-tumoral properties. Heme oxygenase-1 (HO-1) is a stress response protein and is known to play a protective role against the oxidative injury. In this study, we examined whether catalposide could protect Neuro 2A cells, a kind of neuronal cell lines, from oxidative damage through the induction of HO-1 protein expression and HO activity. We also examined the effects of catalposide on the productions of tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ and nitric oxide (NO) on RAW 264.7 macrophages activated with the endotoxin lipopolysaccharide. Methods : HO-1 expression in Neuro 2A cells was measured by Western blotting analysis. NO and $TNF--{\alpha}$ produced by RAW 264.7 macrophage were measured by Griess reagent and enzyme-linked immunosorbent assay, respectively. Results : The treatment of the cells with catalposide resulted in dose- and time-dependent up-regulations of both HO-1 protein expression and HO activity. Catalposide protected the cells from hydrogen peroxide-induced cell death. The protective effect of catalposide on hydrogen peroxide-induced cell death was abrogated by zinc protoporphyrin IX, a HO inhibitor. Additional experiments revealed the involvement of CO in the cytoprotective effect of catalposide-induced HO-1. In addition, catalposide inhibited the productions of $TNF--{\alpha}$ and NO with significant decreases in mRNA levels of $TNF--{\alpha}$ and inducible NO synthase. Conclusions : Our results indicate that catalposide is a potent inducer of HO-1 and HO-1 induction is responsible for the catalposide-mediated cytoprotection against oxidative damage and that catalposide may have therapeutic potential in the control of inflammatory disorders.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.44 no.2
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• pp.111-116
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• 2018

In cosmetics market, anti-pollution products recently come up with new solution for skin health. Environmental oxidation mechanisms are realized as bio-marker of atmospheric pollution upon skin by environmental pollutant such as ozone, UV rays, particulate matter (PM) as well as cigarette smoke. The exposure of cigarette smoke directly or indirectly causes the oxidation of the stratum corneum skin lipids, resulting in the conversion of squalene to squalene monohydroperoxide and/or generation of malondialdehyde (MDA) as a product of lipid peroxidation. The aim of this study is to see whether new cosmetics product containing red beet has anti-oxidation effect on skin exposed by cigarette smoke. So as to determine oxidative damage to human skin at biochemical level, each unit area of volar forearms was exposed to cigarette smoke through device (3.3 cm, diameter) for fifteen minutes, then measured MDA using standardized TBARS assay kit. Compared to negative control (untreated and unexposed area), the level of MDA was significantly increased at positive control (untreated and exposed area) more than 3.7 times, indicating the pollutant induced-oxidative damage on the skin barrier. Whereas, the pre-applied area with the cosmetics products containing red beet revealed a decrease of 25% compared with positive control. As reports, these data demonstrated that cigarette smoke induce peroxidation of stratum corneum skin lipids. Conclusively, we suggest that anti-pollution effect of the cosmetics product containing red beet is beneficial to prevent the oxidation of skin lipids by atmospheric pollution.

• Nutrition Research and Practice
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• v.2 no.2
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• pp.74-79
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• 2008

Zinc plays a protective role in anti-atherosclerosis but the clear mechanism has not been proposed yet. In the present study, we evaluated whether zinc modulates atherosclerotic markers, VACM-1 and ICAM-1 and cell viability both in endothelial cells in vitro and mouse aortic cell viability ex vivo. In study 1, as in vitro model, endothelial EA.hy926 cells were treated with $TNF{\alpha}$ for 5 hours for inducing oxidative stress, and then treated with Zn-adequacy ($15\;{\mu}M$ Zn) or Zn-deficiency ($0\;{\mu}M$ Zn) for 6 hours. Pro-atherosclerosis factors, VCAM-1 and ICAM-1 mRNA expression and cell viability was measured. In study 2, as ex vivo model, mouse aorta ring was used. Mourse aorta was removed and cut in ring then, cultured in a 96-well plate. Aortic ring was treated with various $TNF{\alpha}$ (0-30 mg/ml) and intracellular zinc chelator, N, N, N', N', -tetrakis (2-pyridylmethyl) ethylenediamine (TPEN, $0-30\;{\mu}M$) for cellular zinc depletion for 2 days and then cell viability was measured. The results showed that in in vitro study, Zn-adequate group induced more VCAM-1 & ICAM-1 mRNA expression than Zn-deficient group during 6-hour zinc treatment post-5 hour TNF-$\alpha$ treatment, unexpectedly. These results might be cautiously interpreted that zinc would biologically induce the early expression of anti-oxidative stress through the increased adhesion molecule expression for reducing atherosclerotic action, particularly under the present 6-hour zinc treatment. In ex vivo, mouse aortic ring cell viability was decreased as TNF-$\alpha$ and TPEN levels increased, which suggests that mouse aortic blood vessel cell viability was decreased, when oxidative stress increases and cellular zinc level decreases. Taken together, it can be suggested that zinc may have a protective role in anti-atherosclerosis by cell viability in endothelial cells and aorta tissue. Further study is needed to clarify how pro-atherosclerosis molecule expression is modulated by zinc.