• Korean Journal of Medicinal Crop Science
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• v.16 no.6
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• pp.409-415
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• 2008

Moutan cortex, the root bark of Paeonia suffruticosa Andrews (Paeoniaceae), has pharmacological effects such as anti-inflammatory, antiallergic, analgesic and antioxidant activities. We investigated a methanol extract of Moutan cortex for neuroprotective effects on neurotoxicity induced by amyloid ${\beta}$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons. Exposure of cultured cortical neurons to $10\;{\mu}M\;A{\beta}$ (25-35) for 24 h induced neuronal apoptotic death. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced neuronal cell death at 30 and $50\;{\mu}g/m{\ell}$, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Moutan cortex inhibited $10\;{\mu}M\;A{\beta}$ (25-35)-induced elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) which were measured by fluorescent dyes. Moutan cortex also inhibited glutamate release into medium induced by $10\;{\mu}M\;A{\beta}$ (25-35), which was measured by HPLC. These results suggest that Moutan cortex prevents $A{\beta}$ (25-35)-induced neuronal cell damage by interfering with the increase of $[Ca^{2+}]_i$, and then inhibiting glutamate release and ROS generation. Moutan cortex may have a therapeutic role in preventing the progression of Alzheimer's disease.

• The Journal of Korean Medicine
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• v.17 no.1 s.31
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• pp.9-20
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• 1996

Oxygen free radicals can generated during metabolic processes in normal cells and by exposure of cells to toxic substances. These radicals have been recogenized to playa critical role in several pathological conditions including carcinogenesis and aging, and they have been implicated in pathogenesis of various diseases such as seizure, Alzheimer's disease, Parkinson's disease, myocardial infarction, respiratory distress syndrome, and rheumatoid arthritis. This study was undertaken to determine if Juglandis semen herb-acupuncture solution (JSHAS) has a protective effect against cell injury caused by oxidants, t-butylhydroperoxide (t-BHP) and $H_{2}O_2$. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release and lipid perexidation was estimated by measurimg malondialdehyde, a product of lipid peroxidation. JSHAS significantly prevented LDH release induced by t-BHP or $H_{2}O_2$ in a dose-dependent manner at concentrations of 0.5-10%. Such protective effect was observed in control tissues untreated with oxidants. JSHAS, at 5% concentration, significantly reduced LDH release even when the concentrations of t-BHP and $H_{2}O_2$ increased to 5 and 200 mM, respectively. JSHAS, at 5% concentration, significantly reduced the lipid peroxidation by t-BHP and $H_{2}O_2$. These results indicate that JSHAS prevents cell injury and lipid peroxidation induced by oxidants in rabbit kidney cells. However, the underlying mechanisms remain to determined.

• Journal of Microbiology and Biotechnology
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• v.26 no.2
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• pp.277-286
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• 2016

Makgeolli lees (ML) has several physiological effects such as antioxidant, antidiabetic, and anticancer properties, but its biological functions have not been determined definitively. Here, we tested whether ML has a cytoprotective effect on paraquat (PQ)-induced oxidative stress in the human lung carcinoma cell line A549. At 0.1 mg/ml ML, viability of PQ-exposed A549 cells was restored by 12.4%, 18.5%, and 48.6% after 24, 48, and 72 h, respectively. ML also reduced production of the intracellular reactive oxygen species (ROS) that were generated by PQ treatment. Further experiments revealed that ML treatment enhanced the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) as well as ARE-GFP reporter activity. ML treatment also effectively increased the expression of NRF2's target genes NAD(P)H dehydrogenase quinone 1 (NQO1) and heme oxygenase 1 (HO-1). Moreover, we found that expression of cytoprotective genes, including glutathione peroxidases (GPXs), superoxide dismutase (SOD1), catalase (CAT), peroxiredoxin 3 (PRDX3), and peroxiredoxin 4 (PRDX4), was greatly enhanced by treatment with ML during PQ exposure. Taken together, the data suggest that treatment of PQ-exposed A549 cells with ML ameliorates cytotoxicity through induction of NRF2 expression and its target genes HO-1, NQO1, and other antioxidant genes. Thus, ML may serve as a functional food applicable to ROS-mediated human diseases.

• ETRI Journal
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• v.16 no.1
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• pp.45-57
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• 1994

The effects of reactive ion etching (RIE) of $SiO_2$ layer in $CHF_3/C_2F_6$ on the underlying Si surface have been studied by X-ray photoelectron spectroscopy (XPS), secondary ion mass spectrometer, Rutherford backscattering spectroscopy, and high resolution transmission electron microscopy. We found that two distinguishable modified layers are formed by RIE : (i) a uniform residue surface layer of 4 nm thickness composed entirely of carbon, fluorine, oxygen, and hydrogen with 9 different kinds of chemical bonds and (ii) a contaminated silicon layer of about 50 nm thickness with carbon and fluorine atoms without any observable crystalline defects. To search the removal condition of the silicon surface residue, we monitored the changes of surface compositions for the etched silicon after various post treatments as rapid thermal anneal, $O_2$, $NF_3$, $SF_6$, and $Cl_2$ plasma treatments. XPS analysis revealed that $NF_3$ treatment is most effective. With 10 seconds exposure to $NF_3$ plasma, the fluorocarbon residue film decomposes. The remained fluorine completely disappears after the following wet cleaning.

• Journal of Ginseng Research
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• v.44 no.2
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• pp.267-273
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• 2020

Background: Continuous exposure to high temperatures can lead to heat stress. This stress response alters the expression of multiple genes and can contribute to the onset of various diseases. In particular, heat stress induces oxidative stress by increasing the production of reactive oxygen species. The liver is an essential organ that plays a variety of roles, such as detoxification and protein synthesis. Therefore, it is important to protect the liver from oxidative stress caused by heat stress. Korean ginseng has a variety of beneficial biological properties, and our previous studies showed that it provides an effective defense against heat stress. Methods: We investigated the ability of Korean Red Ginseng and Korean black ginseng extracts (JP5 and BG1) to protect against heat stress using a rat model. We then confirmed the active ingredients and mechanism of action using a cell-based model. Results: Heat stress significantly increased gene and protein expression of oxidative stress-related factors such as catalase and SOD2, but treatment with JP5 (Korean Red Ginseng extract) and BG1 (Korean black ginseng extract) abolished this response in both liver tissue and HepG2 cells. In addition, JP5 and BG1 inhibited the expression of inflammatory proteins such as p-NF-κB and tumor necrosis factor alpha-α. In particular, JP5 and BG1 decreased the expression of components of the NLRP3 inflammasome, a key inflammatory signaling factor. Thus, JP5 and BG1 inhibited both oxidative stress and inflammation. Conclusions: JP5 and BG1 protect against oxidative stress and inflammation induced by heat stress and help maintain liver function by preventing liver damage.

• Molecules and Cells
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• v.39 no.6
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• pp.508-513
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• 2016

To investigate the potential therapeutic effects of polyphenols in treating Pb induced renal dysfunction and intoxication and to explore the detailed underlying mechanisms. Wistar rats were divided into four groups: control groups (CT), Pb exposure groups (Pb), Pb plus Polyphenols groups (Pb+PP) and Polyphenols groups (PP). Animals were kept for 60 days and sacrificed for tests of urea, serum blood urea nitrogen (BUN) and creatinine. Histological evaluations were then performed. In vitro studies were performed using primary kidney mesangial cells to reveal detailed mechanisms. Cell counting kit-8 (CCK-8) was used to evaluate cell viability. Pb induced cell apoptosis was measured by flow cytometry. Reactive oxygen species (ROS) generation and scavenging were tested by DCFH-DA. Expression level of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-1-${\beta}$ (IL-1-${\beta}$) and IL-6 were assayed by ELISA. Western blot and qPCR were used to measure the expression of ERK1/2, JNK1/2 and p38. Polyphenols have obvious protective effects on Pb induced renal dysfunction and intoxication both in vivo and in vitro. Polyphenols reduced Pb concentration and accumulation in kidney. Polyphenols also protected kidney mesangial cells from Pb induced apoptosis. Polyphenols scavenged Pb induced ROS generation and suppressed ROS-mediated ERK/JNK/p38 pathway. Downstream pro-inflammatory cytokines were inhibited in consistency. Polyphenol is protective in Pb induced renal intoxication and inflammatory responses. The underlying mechanisms lie on the antioxidant activity and ROS scavenging activity of polyphenols.

• Korean Journal of Medicinal Crop Science
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• v.17 no.6
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• pp.388-396
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• 2009

The present study investigated an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix for possible neuroprotective effects on neurotoxicity induced by amyloid $\beta$ protein ($A{\beta}$) (25-35) in cultured rat cortical neurons and antidementia activity in mice. Exposure of cultured cortical neurons to $10\;{\mu}M$ $A{\beta}$ (25-35) for 36 h induced neuronal apoptotic death. At $1-50\;{\mu}g/m{\ell}$, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $A{\beta}$ (25-35) in primary cultures of rat cortical neurons. Memory loss induced by intracerebroventricular injection of ICR mice with 15 nmol $A{\beta}$ (25-35) was inhibited by chronic treatment with HS0608 (25, 50 and 100 mg/kg, p.o. for 7 days) as measured by a passive avoidance test. From these results, we suggest that the antidementia effect of HS0608 is due to its neuroprotective effect against $A{\beta}$ (25-35)-induced neurotoxicity and that HS0608 may have a therapeutic role in preventing the progression of Alzheimer's disease.

• Korean Journal of Medicinal Crop Science
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• v.15 no.6
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• pp.444-450
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• 2007

Dried leaves from Cedrela sinensis A. Juss. (CS), have been observed to possess various pharmacological activity and contain various antioxidant constituents. The protective effect of ethanol extract of CS on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity was examined using primary cultured rat cortical neurons in the present study. Exposure of cultured neurons to 100 ${\mu}M\;H_2O_2$ caused a significant neuronal death as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. The addition of CS, over a concentration range of 10 to $50{\mu}g/m{\ell}$, concentration-dependently prevented the $H_2O_2-induced$ neuronal apoptotic death. CS $(50{\mu}g/m{\ell})$ significantly inhibited $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, Fluo-4 AM. CS (30 and $50{\mu}g/m{\ell})$ inhibited glutamate release and generation of reactive oxygen species (ROS) induced by $100{\mu}M\;H_2O_2$. These results suggest that CS may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

• Journal of Korean Biological Nursing Science
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• v.3 no.1
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• pp.53-61
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• 2001

Skin is constantly exposed to air, solar radiation, ozone and other air pollutants formulating free radicals. The reactive oxygen species(ROS), formed under these conditions, are associated with skin cancers, cutaneous photoaging, and cutaneous inflammatory disorders. In this study, we sought to establish an animal model for UVB-induced skin alteration using BALB/c mice. The level of UVB irradiation used in this model was within physiological dose. BALB/c mice were exposed to a single dose of UVB ($200mJ/cm^2$ and were sacrificed at 3, 6, 24, and 48 hours following the irradiation. The effect of a single exposure to UVB irradiation on skin catalase(CAT), superoxide dismutase(SOD), and glutathione peroxidase(GPx) activities were examined. Significant decrease in the activity of all enzymes were observed at 6 hours after irradiation(p<.05). The activity of CAT decreased more sharply than those of SOD and GPx, and then remained depressed until 48 hours after UVB irradiation, whereas the activity of GPx recovered to basal level at 48 h after UVB irradiation. Our results indicate that BALB/c mouse could be an adequate animal model of UVB irradiation experiment. These results will also provide fundamental knowledge for the effective nursing strategies in reducing UV-induced skin disorders.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.376-382
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• 2011

Background: Carbon monoxide (CO) is a cytoprotective and homeostatic molecule with important signaling capabilities in physiological and pathophysiological situations. CO protects cells/tissues from damage by free radicals or oxidative stress. NAD(P)H:quinone oxidoreductase (NQO1) is a highly inducible enzyme that is regulated by the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, which is central to efficient detoxification of reactive metabolites and reactive oxygen species (ROS). Methods: We generated NQO1 promoter construct. HepG2 cells were treated with CO Releasing Molecules-2 (CORM-2) or CO gas and the gene expressions were measured by RT-PCR, immunoblot, and luciferase assays. Results: CO induced expression of NQO1 in human hepatocarcinoma cell lines by activation of Nrf2. Exposure of HepG2 cells to CO resulted in significant induction of NQO1 in dose- and time-dependent manners. Analysis of the NQO1 promoter indicated that an antioxidant responsible element (ARE)-containing region was critical for the CO-induced Nrf2-dependent increase of NQO1 gene expression in HepG2 cells. Conclusion: Our results suggest that CO-induced Nrf2 increases the expression of NQO1 which is well known to detoxify reactive metabolites and ROS.