• The Journal of Korean Medicine
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• v.21 no.2
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• pp.79-86
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• 2000

Objectives and Methods : In order to elucidate toxic mechanism of myocardial damage and protective effect of myrrha water extract against cytotoxic effect of xanthine oxidase/hypoxanthine(XO/HX), cardioprotective effect of myrrha water extract was examined by MTT assay, LDH (Lactate Dehydrogenase) activity and heart beating rate after cultured myocardial cells derived from neonatal mouse were treated with various concentration of XO/HX, a free radical. Results : XO/HX induced a decrease of cell viability, an increase in the amount of LDH, and a decrease of heart beating rate on cultured myocardial cells in a dose-dependent manner. In cardioprotective effect of myrrha water extract, it showed a decrease in the amount of LDH and an increase of heart beating rate on cultured myocardial cells damaged by XO/HX. Conclusions : From the above results, it is suggested that XO/HX showed toxic effect in cultured myocardial cells derived from neonatal mouse and that myrrha water extract is very effective in the prevention of XO/HX-induced cardiotoxicity.

• Journal of Nutrition and Health
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• v.33 no.7
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• pp.739-744
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• 2000

The purpose of this study was to elucidate protective effect of Fructus Schsandrae(FS) water extract against xanthine oxidase/hypoxanthine(XO/HX)-induced cardiotoxicity in myocardial cells this experiment was performed. Cardiotoxicity of XO/HX was examined by MTT(MTT [3-(4,5-dimethylthiazol-2-yl)-2.5,-diphenyl tetrazolium bromide) assay. XO/HX induced the decrease of cell viability. Also XO/HX induced the increase of LDH activity and the decrease of beating rate on cultured myocardial cells in a dose-dependent manner. To investigate cardioprotective effect of FS water extract cultures were preincubated with FS water extract for 3 hours. Cultures were then exposed to XO/HX for 72 hours. FS water extract have an efficacy in decreaasing LDH activity and increasing heart beating rate on cultured myocardial cells damaged by XO/HX. From the results it is suggested that XO/HX may show toxic effect in cultured myocardial cells derived from neonatal mouse and FS water extract is effective in the prevention of XO/HX-induced cardiotoxicity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1231-1234
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• 2003

To clerify the toxic effect of methylmercuric chloride(MMC) in cultured mouse myocardial cells, cytotoxic effect was measured by MTT assay after cultured myocardial cells were incubated for 48 hours in the media containing 1～30 uM concentrations of MMC. And also, the protective effect of Benincasae Semen (BS) was assessed in these cultrures. Cell viability was significantly decreased in a dose-dependent manner after cultured myocardial cells were exposed to 30 uM MMC for 48 hours. In the neuroprotective effect of BS on MMC-induced cytotoxicity, BS blocked the MMC-induced myotoxicity in these cultures. From these results, it suggests that MMC is toxic on cultured mouse myocardial cells and BS is effective in blocking the neurotoxicity induced by MMC.

• The Journal of Korean Medicine
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• v.20 no.1 s.37
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• pp.142-150
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• 1999

In order to elucidate toxic the mechanism of myocardial damage and the protective effect of herbal extract, Sophorae Radix(SR) against myocardiotoxicity, the cytotoxic effect of adriamycin and cardioprotective effect of SR were examined by MTT assay, LDH activity, heart beat rate and light microscopy after cultured myocardial cells derived from neonatal mouse were treated with various concentrations of adriamycin, an inducer of myocardiotoxicity. Adriamycin induced a decrease of cell viability, an increase in the amount of lactate dehydrogenase(LDH), and a decrease in the heart beat rate and a decrease in the number of cells, when administered to cultures myocardial cells in a dose-dependent manner. In cardioprotective effect of SR. SR showed the decrease of amount of LDH, and an increase of heart beating rate and cells in number on cultured myocardial cells damaged by adriamycin. From the above results, it is suggested that adriamycin shows toxic effect in cultured myocardial cells derived from a neonatal mouse, and herbal extract such as SR is very effective in the prevention of adriamycin-induced cardiotoxicity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1197-1200
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• 2002

To examine the cardiotoxicity of glucose oxidase(GO) in cultured myocardial cells, cardiotoxicity was measured by MTT assay. Myocardial cells were treated with 1～50 mU/ml GO for 5 hours. The cardioprotective effect of Benincasae Semen(BS) was measured by MTT assay in these cultrures. Cell viability was significantly decreased in dose- and time-dependently after myocardial cells were exposed to 30mU/ml GO for 5 hours. In the cardioprotective effect of BS on the cardiotoxicity induced by GO, BS prevented the cardiotoxicity induced by GO in these cultures. From these results, it suggests that GO had cytotoxic effect in cultured myocardial cells and herb extract, BS showed protective effect on GO-induced cardiotoxicity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.3
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• pp.495-498
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• 2002

Cytotoxicity of glucose oxidase(GO) and neuroprotective effect of Aconiti Radix(AKR) against GO-induced neurotoxicity were measured for elucidating the mechanism of cardiotoxicity on cultured mouse myocardial cells by MTT assay after myocardial cells were cultured for 24 hours at various concentrations of GO. GO was toxic in a time-and dose-dependent manner on cultured myocardial cells after myocardial cells were grown for 24 hours in media containing 5～40mU/ml GO. While, cultures were pretreated with 50 μg/ml AKR for 2 hours increased remarkably cell viability. From the above results, it is suggested that GO is toxic on cultured mouse myocardial cells by the decrease of cell viability, and herb medicine such as AKR is very effective in the prevention of myocardial toxicity induced by GO.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1207-1210
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• 2002

To examine the cardiotoxic effect of adriamycin on cultured rat myocardial cells, cytotoxicity was measured by MTT assay after cultured myocardial cells were grown with various concentrations of adriamycin(ADA) for 48 hours. The protective effect of Benincasae Semen(BS) on ADR-induced cardiotoxicity was also examined in these cultures. ADR decreased cell viability of cultured rat myocardial cells remarkably in a dose- and time-dependent manners. In protective effect of BS, it was very effective in blocking ADR-induced cytotoxicity. From these results, it is suggested that ADR shows cardioxicity, and the herba extract, as is very effective in preventing ADR-induced cytotoxicity on cultured rat myocardial cells.

• The Journal of Internal Korean Medicine
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• v.21 no.1
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• pp.46-54
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• 2000

Objectives : Talmyung-san(TMS) has been used for treatment of brain diseases in Chinese traditional medicine. However, little is known about the mechanism by which TMS rescues brain cells from ischemic damages. To elucidate the protective mechanisms of TMS, we execute experiments. Methods : The effects of TMS on ischemia/reperfusion-induced cytotoxicity and generation of nitric oxide(NO) are investigated in primary neonatal myocardial cells and A7rS, aortic smooth muscle cell line. Results : Ischemia/reperfusion itself induces severe myocardial cell death in vitro. However, treatment of the cells with TMS significantly reduces both ischemia/reperfusion-induced myocardial cell death and LDH release. In addition, pretreatment of TMS before reperfusion recovers the lose of beating rates alter ischemia/reperfusion. For a while, the water extract of TMS stimulates myocardial cells to produce NO in a dose dependent manner and it protects the damage of ischemia/reperfusion-induced myocardial cells. Furthermore, the protective effects of the water extract of TMS is mimicked by treatment of sodium nitroprusside, an exogenous NO donor. NG-monomethyl-L-arginine (NGMMA), a specific inhibitor of nitric oxide synthase(NOS), significantly blocks the protective effects of TMS on the cells after ischemia/reperfusion. In addition, on ischemia the water extract of TMS induce NO in A7r5 cell. Conclusions : Taken together, we suggest that the protective effects of TMS against ischemia/reperfusion-induced myocardial damages may be mediated by NO production of myocardial and vascular smooth muscle cell during ischemic condition.

• The Journal of Korean Medicine
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• v.19 no.2
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• pp.100-111
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• 1998

This study is designed to investigate the effects of Saengmaegsan extract on cultured myocardial cell sheets affected by oxygen tension change. The results were as follows : 1. Saengmaegsan meaningfully restored the cellular activity decrease in the cultured myocardial cells affected by high oxygen tension. 2. Saengmaegsan meaningfully lessened the degree of total protein decrease in the myocardial cells caused by high oxygen tension. 3. Saengmaegsan meaningfulJy refrained from syntetic decrease of 4-hydroxyproline in both low oxygen tension group and high oxygen tension group.

• Journal of Chest Surgery
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• v.29 no.4
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• pp.365-372
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• 1996

In an attempt to evaluate the effect of St. Thomas' hospital cardioplegic solution (STH) I and II on the cultured rat myocardial cells, beating rate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (Irtrazolium MTT) and lactate dehydrogenase activity were investigated, and also light and electron microscopic studies were carried out. After rat myocardial cells were cultured for 72 hours, cells were treated with STH I or with STH H solution for 30 and 120 min. and thereafter myocardial cells were cultured in control medium for 24 hours. The results obtained were as follows : 1. Beating rate was 154 times per min. in control group, 141 times per min. in STH I solution(for 2. 120 min.)-treated group and 145 times in STH ll solution (for 120 min.)-treated group. MTT absorbances by MTT assay were 102% in STH I solution (for 120 min.)-treated group and 93% in STH ll solution (for 120 min.)-treated group compared with control group. 3. The amount of lactate dehydrogenase released into the medium were 123% in STH I solution (for 120 min.)-treated group and 109% in STH H solution (for 120 min.)-treated group compared with control group. 4. In the light microscopy examination, myocardial cells showed no differences between experimental and control groups in their number and shape. 5. In the electron microscopy examination, myocardial cells treated with STH I solution showed fewer destroyed mitochondria compared to STH ll solution-treated group. These results suggest that both 51. Thomas'cardioplegic solution STH 1 and STH H have no cytotoxicity on cultured rat myocardial cells, but STH H solution has more protective effect on myocardial cells compared to STH I solution.