• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1202-1207
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• 2003

In order to clarify the neuroprotective effect of Cornu Saigae Tataricae(CST) water extract on cultured mouse spinal motor neuron damaged by hydrogen peroxide (H₂O₂), MTT [3-(4,5-dimethylthiazole-2-yl)- 2,5-diphenyltetrazolium bromide] assay, LDH (Lactate Dehydrogenase) activity assay and SRB (Sulforhodamine B) assay were carried out after the cultured mouse spinal motor neuron were preincubated with various concentrations of CST water extract for 3 hours prior to exposure of hydrogen peroxide Cell viability of cultured mouse spinal motor neurons exposed to various concentrations of hydrogen peroxide for 6 hours was decreased in a dose-dependent manner. MTT50 values were 40 uM hydrogen peroxide. Cultured mouse spinal motor neurons in the medium containing various concentration of hydrogen peroxide for 6 hours showed increasing of LDH activity and decreasing of total protein synthesis. We know that hydrogen peroxide was toxic on cultured spinal motor neurons. Pretreatment of CST water extract for 3 hours following hydrogen peroxide prevented the hydrogen peroxide-induced neurotoxicity such as increasing of LDH activity and decreasing of total protein synthesis. These results suggest that hydrogen peroxide shows toxic effect on cultured spinal motor neurons and CST water extract is highly effective in protecting the neurotoxicity induced by hydrogen peroxide.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6301-6306
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• 2014

Cervical cancer is one the most common malignancies among females. In recent years, its incidence rate has shown a rising trend in some countries so that development of anticancer drugs for cervical cancer is an urgent priority. In our recent anticancer drug discovery screen, 1, 2-di (quinazolin-4-yl)diselane (LG003) was found to possess wide spectrum anticancer efficacy. In the present work, the in vitro anticancer activity of LG003 was evaluated in the SiHa cervical cancer cell line. Compared with commercial anticancer drugs 10-hydroxycamptothecin, epirubicin hydrochloride, taxol and oxaliplatin, LG003 showed better anticancer activity. Furthermore, inhibition effects were time- and dose-dependent. Morphological observation exhibited LG003 treatment results in apoptosis like shrinking and blebbing, and cell membrane damage. Lactate dehydrogenase release assay revealed that LG003 exerts such effects in SiHa cells through a physiology pathway rather than cytotoxicity, which suggests that title compound LG003 can be a potential candidate agent for cervical cancer.

• Restorative Dentistry and Endodontics
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• v.19 no.2
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• pp.409-428
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• 1994

Endodontic surgery is performed when conventional endodontic therapy fails or is contraindicated. In such cases, retrograde filling materials including amalgam, composite resin, and various cements have been used. Biocompatibilty and margin sealing ability of retrograde filling materials are important for the long term success of endodontic surgery. In vitro cell culture is frequently used as the method of measuring the biocompatibilty of dental materials. The purpose of this study was to evaluate the cytotoxicity of six kinds of retrograde filling materials including newly developed light curing glass ionomer cements. Each material was mixed according to. the manufacture's instruction and evaluated as : freshly mixed, 24-hour after mixing, and 168-hour after mixing respectively. The elution solution was extracted after 24-hour contact with materials using media. Cytotoxicity was evaluated by direct contact, or elution contact. Test results of radiochromium($^{51}Cr$) release, cell viability using tetrazolium dye (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl dimethyltetrazolium bromide(MTT) test and lactate dehydrogenase(LD) of damaged L929 cells were analyzed. In the $^{51}Cr$ release of direct contact, all experimental retrograde filling materials except amalgam and glass ionomer cement showed increased cytotoxicity compared to control. In the $^{51}Cr$ release of elution solution, the released $^{51}Cr$ was so minimal that it was impossible. to evlauate the cytotoxicity exactly. The elution solutions of glass ionomer cement and IRM showed marked cytotoxicity in MTT test. LD enzyme activity was highest in tests of direct contact with composite, light curing composite, and light curing glass ionomer cement and IRM. Amalgam revealed least cytotoxicity while IRM showed cytotoxicity using all three methods. Composite, light curing composite and light curing glass iomomer cement were cytotoxic in the tests of $^{51}Cr$ release and LD activity. Glass ionomer cement showed cytotoxic effect only in the MTT method. From these results it is suggested that the standardization and optimization of cytotoxicity testing, especially using elution solutions, should be strongly advised.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.27 no.3
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• pp.193-200
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• 2017

Objectives: This study was performed to evaluate the neurototoxicity of the environmental pollutant lead acetate(LA) and the protective effect of the D-2-amino-5-phosphonovaleric acid(APV), N-methyl-D-aspartate(NMDA) receptor antagonist on LA-induced cytotoxicity in cultured C6 glioma cells. Materials and Methods: For this study, cell viability in cultured C6 glioma cells was assessed by XTT assay and antioxidative effect, such as lactate dehydrogenase(LDH) activity, by LDH detection kit. Results: LA significantly decreased cell viability in a dose-dependent manner, and the XTT50 value was determined to be 33.3 uM of LA. The cytotoxicity of LA was deemed highly toxic according to Borenfreund and Puerner's toxic criteria. The vitamin E antioxidant significantly increased cell viability damaged by LA-induced cytotoxicity in these cultures. For the protective effect of APV on LA-induced cytotoxicity, APV significantly increased not only cell viability, but also inhibition of LDH activity. From these results, it is suggested that oxidative stress is involved in the neurotoxicity of LA, and APV effectively protected against LA-induced cytotoxicity via an antioxidative effect as an inhibotory activity of LDH. Conclusions: Natural resources like APV may be putative therapeutic agents for the toxic diminution of environmental pollutants such as LA correlated with oxidative stress.

• Korean Journal of Agricultural Science
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• v.47 no.3
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• pp.497-508
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• 2020

In this study, we investigated the protective effects of 'Donganme' (Sorghum bicolor L. Moench) against oxidative stress under in vitro conditions and in a cellular system using C6 glial cells. The radical scavenging activities were observed using the substrates 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl (•OH) radicals. The Donganme extract had an •OH radical scavenging activity of 82.66% at a concentration of 100 ㎍·mL^-1. Additionally, when DPPH was used as the substrate, the Donganme extract exhibited a strong radical scavenging activity in a concentration-dependent manner with an IC₅₀ value of 28.56 ㎍·mL^-1. Furthermore, treating C6 glial cells with hydrogen peroxide (H₂O₂) reduced the cell viability and generated reactive of oxygen species (ROS) and lactate dehydrogenase (LDH) compared to the normal levels, indicating that H₂O₂ induced oxidative stress. However, Donganme extracts increased the cell viability and inhibited ROS and LDH production against oxidative stress by H₂O₂ in the C6 glial cells. In particular, it showed effective cell protection with the cell viability, ROS production, and LDH release at 83.50, 88.06, and 14.87%, respectively, which were lower than the control or similar to the normal levels even at a low concentration of 100 ㎍·mL^-1. The present study suggests that the Donganme extract was effective in protecting against oxidative stress in C6 glial cells through its antioxidant activity. Thus, Donganme could be a promising therapeutic agent for neurodegenerative diseases due to oxidative stress.

• Korean Journal of Pharmacognosy
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• v.41 no.3
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• pp.166-173
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• 2010

Oxidative stress to proteins, lipids, or DNA is higher in human autopsy tissue and in rodent models of a number of neurodegenerative conditions, including Alzheimer's and Parkinson's disease. On the basis of this information, we established a screening system using N18-RE-105 cells to identify therapeutic agents that can protect cells from glutamate toxicity. During the course of our screening program, we recently isolated the active compound 9-hydroxy-$\alpha$-tocopherone ($\alpha$-TP), which prevents glutamate-induced cell death, from Viola mandshurica. The chemical structure of $\alpha$-TP was identified using spectroscopic methods and by comparison with literature values. Antioxidant activity and protective effects of $\alpha$-TP were evaluated by DPPH radical-scavenging assay, morphological assay, MTT reduction assay, and lactate dehydrogenase (LDH) release assay. These results suggest that $\alpha$-TP could be a new potential chemotherapeutic agent against neuronal diseases.

• Archives of Pharmacal Research
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• v.28 no.12
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• pp.1358-1364
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• 2005

In this study, we investigated whether a novel anti-ischemic $K_{ATP}$ opener KR-31378 [(2S,3S,4R)­N'-cyano-N-(6-amino-3,4-dihydro-3-hydroxy-2 -methly-2-dimethoxymethly-2H-benzopyran-4-yl)­N'-benzylguanidine] has protective effect against oxidative stress-induced death in heart-derived H9c2 cells. Cell death was induced by BSO, butionine sulfoximine, which inhibits GSH synthesis and subsequently increases reactive oxygen species (ROS) level. Cell death was quantitatively determined by measuring lactate dehydrogenase (LDH) activity and stained by Hoechst 33258. BSO-induced ROS production and mitochondrial membrane potential (MMP) were measured using 2',7'-dichlorofluorescein diacetate oxidation and rhodamine 123, respectively. Both the LDH release and the ROS elevation induced by treatment of H9c2 cells with 10 mM BSO, were significantly decreased by KR-31378. These protective effect and antioxidant effect of KR-31378 appeared to be independent on $K_{ATP}$ channel opening. Cells exposed to BSO showed an early reduction in MMP, and this reduction in MMP was significantly reversed by treatment with KR-31378. Caspase-3 activity in BSO treated H9c2 cells was remarkably increased, and this increased caspase-3 activity was significantly reversed by KR-31378. In conclusion, our results suggest that KR-31378 can produce cardioprotective effect against oxidative stress-induced cell death through antioxidant mechanism.

• Toxicological Research
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• v.35 no.1
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• pp.83-91
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• 2019

Nanoparticles (NPs) have been recognized as both useful tools and potentially toxic materials in various industrial and medicinal fields. Previously, we found that zinc oxide (ZnO) NPs that are neurotoxic to human dopaminergic neuroblastoma SH-SY5Y cells are mediated by lipoxygenase (LOX), not cyclooxygenase-2 (COX-2). Here, we examined whether human bone marrow-derived mesenchymal stem cells (MSCs), which are different from neuroblastoma cells, might exhibit COX-2- and/or LOX-dependent cytotoxicity of ZnO NPs. Additionally, changes in annexin V expression, caspase-3/7 activity, and mitochondrial membrane potential (MMP) induced by ZnO NPs and ZnO were compared at 12 hr and 24 hr after exposure using flow cytometry. Cytotoxicity was measured based on lactate dehydrogenase activity and confirmed by trypan blue staining. Rescue studies were executed using zinc or iron chelators. ZnO NPs and ZnO showed similar dose-dependent and significant cytotoxic effects at concentrations ${\geq}15{\mu}g/mL$, in accordance with annexin V expression, caspase-3/7 activity, and MMP results. Human MSCs exhibited both COX-2 and LOX-mediated cytotoxicity after exposure to ZnO NPs, which was different from human neuroblastoma cells. Zinc and iron chelators significantly attenuated ZnO NPs-induced toxicity. Conclusively, these results suggest that ZnO NPs exhibit both COX-2- and LOX-mediated apoptosis by the participation of mitochondrial dysfunction in human MSC cultures.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.5
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• pp.808-813
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• 2002

This study investigated the effects of different kinds of dietary fibers, cellulose, psyllium husk, pectin and the Psyllium husk Plus Pectin, on the lipid concentration and hernobiochemical enzyme activity in male Sprague-Dawley rats. The experimental groups were divided into four groups : the cellulose group, the psyllium husk group, the pectin group and the psyllium husk Plus Pectin group. Dietary fiber was supplemented at 10% (w/w) levels in the diet. Body weight gain, food intake and relative tissue seight were not significantly different among the dietary groups. Concentrations of triglyceride and phospholipid of serum in the psyllium husk and the pectin groups were significantly lower than those of the cellulose and the psyllium husk plus pectin groups. Concentration of total cholesterol of serum in the psyllium husk plus pectin group was lower than other dietary groups. However, concentrations of triglyceride and phospholipid of liver in the psyllium husk and the pectin groups were significantly higher than those of the cellulose and the psyllium husk plus pectin groups. The hemobiochemical Parameters, total protein, albumin, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase, alkaline phosphatase, lactate dehydrogenase and blood urea nitrogen in serum of the psyllium husk group were lower than other dietary groups. These results showed that dietary psyllium husk could have lowering effects on serum triglyceride concentration without any side effect of hemobiochemical enzyme activity in rats.

• Journal of Ginseng Research
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• v.37 no.3
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• pp.273-282
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• 2013

The present study was designed to investigate the cardioprotective effects of Korean Red Ginseng extract (KRG) on isoproterenol (ISO)-induced cardiac injury in rats, particularly in regards to electrocardiographic changes, hemodynamics, cardiac function, serum cardiac enzymes, components of the myocardial antioxidant defense system, as well as inflammatory markers and histopathological changes in heart tissue. ISO (150 mg/kg, subcutaneous, two doses administered at 24-hour intervals) treatment induced significant decreases in P waves and QRS complexes (p<0.01), as well as a significant increase in ST segments. Moreover, ISO-treated rats exhibited decreases in left-ventricular systolic pressure, maximal rate of developed left ventricular pressure ($+dP/dt_{max}$) and minimal rate of developed left ventricular pressure ($-dP/dt_{max}$), in addition to significant increases in lactate dehydrogenase, aspartate transaminase, alanine transaminase and creatine kinase activity. Heart rate, however, was not significantly altered. And the activities of superoxide dismutase, catalase and glutathione peroxidase were decreased, whereas the activity of malondialdehyde was increased in the ISO-treated group. ISO-treated group also showed increased caspase-3 level, release of inflammatory markers and neutrophil infiltration in heart tissue. KRG pretreatment (250 and 500 mg/kg, respectively) significantly ameliorated almost all of the parameters of heart failure and myocardial injury induced by ISO. The protective effect of KRG on ISO-induced cardiac injury was further confirmed by histopathological study. In this regard, ISO treatment induced fewer morphological changes in rats pretreated with 250 or 500 mg/kg of KRG. Compared with the control group, all indexes in rats administered KRG (500 mg/kg) alone were unaltered (p>0.05). Our results suggest that KRG significantly protects against cardiac injury and ISO-induced cardiac infarction by bolstering antioxidant action in myocardial tissue.