• The Journal of Korean Medicine
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• v.23 no.3
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• pp.174-187
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• 2002

Objectives : This study was carried out to determine whether Kamihaengche-tang plus Yulanijihwang-tang (KCYH) exerts a protective effect against oxidant-induced liver cell injury. Methods : Cell injury was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. Results : Oxidants (tBHP and $H_2O_2$) increased dose-dependently LDH release which was significantly prevented by 1% KCYH. The protective effect of KCYH against oxidant-induced cell injury was dose-dependent in the range of 0.05-1 % concentrations. Similarly, KCYH inhibited oxidant-induced lipid peroxidation in a dose-dependent manner. When liver tissues were exposed to Hg (0.5 mM), ALT activity in the medium and lipid peroxidation in tissues were markedly increased. These changes were prevented by 1% KCYH, KCYH restored toxicant-induced inhibition of cellular GSH content. KCYH increased the activities of catalase and glutathion peroxidase in oxidant-treated tissues. Conclusions : These results indicate that KCYH exerts a protective effect against oxidant-induced liver cell injury, and this effect is attributed to prevention of lipid peroxidation. These effects may be due to an increase in concentration of endogenous antioxidants.

• Journal of Acupuncture Research
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• v.19 no.5
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• pp.209-218
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• 2002

Objective : This study was undertaken to examine whether Carthami Semen aquacupuncture (CSA) exerts protective effect against Hg-induced cell injury in rabbit liver. Methods : The cell injury was evaluated by ALT activity and lipid peroxidation was estimated by measuring malondialdehyde (MDA). Results : Hg caused an increase of ALT activity and lipid peroxidation in a dose-dependent-manner over concentrations of 0.1-1 mM, which were prevented by addition of 0.005% CSA. The protective effect of CSA was dose-dependent in concentration range of 0.001 to 0.01%. The increase of ALT activity and lipid peroxidation induced by 0.5 mM Hg were almost completely decreased by addition of 0.01% CSA. When the liver tissues were exposed to 0.5 mM Hg, GSH content was decreased, which was significantly restored by 0.01% CSA. 0.5 mM Hg caused decrease in the amount of total and nonprotein sulfhydryl groups, and 0.01% CSA prevented Hg-induced reduction of nonprotein sulfhydryl group but not protein sulfhydryl group. Conclusions : These results suggest that CSA exerts protective effect against Hg-induced cell injury by antioxidant action resulting from enhancement of nonprotein sulfhydryl group content including GSH in liver.

• Journal of Life Science
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• v.8 no.4
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• pp.464-471
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• 1998

This study was carried out to determine whether Kamihaengche-tang plus Yukmijihwang-tang (KCYH) exerts the protective effect against oxidant-induced liver cell injury. Cell injurt was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. $H_2O_2$increased LDH release which was significantly prevented by 1% KCYHT. The protective effect of KCYH against $H_2O_2$-induced cell injury was dose-dependent in the range of 0.05-1% concentrations. Similary, KCYH inhibited $H_2O_2$ induced lipid peroxidation in a dose-dependent manner. When liver tissuse were exposed to Hg(0.5 mM), ALT activity in the medium and lipid erpoxidation in tissues were markedly increased. These changes were prevented by 1% KCYH. KCHY restored Hg-induced inhibition of cellular GSH content. These result indicate that KCYH exerts the protective effect oxidant-induced liver cell injury, and this effect is attributed to prevented to prevention of lipid peroxidation. These dffects may be due to an increase in concentration of endogenous antioxidants.

• The Journal of Korean Medicine
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• v.24 no.3
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• pp.96-107
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• 2003

Objective : This study was undertaken to determine if Pyunggangaeuljihyul-tang (Pinggankaiyuzhixue-tang, PG) has a protective effect against cell injury induced by various toxic agents in rabbit liver, Methods : Cell injury in vitro was estimated by measuring lactate dehydrogenase (LDH), and that in vivo was estimated by measuring alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity in serum. Lipid peroxidation was examined by measuring malondialdehyde, a product of lipid per oxidation. Results : PG prevented the LDH release by $CCl_4$, mercury, menadione, and tert-butyl hydroperoxide treatment in vitro in liver slices. The extent of protection by 2% PG was similar to that of $10{\mu\textrm{M}}$ N,N'-diphenyl-p-phenylenedianline, a potent antioxidant, in tert-butyl hydroperoxide-induced LDH release. PG also prevented lipid peroxidation and depletion of cellular ATP induced by Hg. Hg causes motphological changes including cell necrosis and its effect was significantly prevented by PG. When rats were treated intraperitoneatly with 0.5 ml/kg of $CCl_4$, serum alanine aminotransferase and aspartate aminotransferase activities were increased compared with the control, which was significantly inhibited by pretreatment of PG. PG also prevented reduction in GSH and lipid peroxidation induced by $CCl_4$ Conclusion : These results suggest that PG exerts aprotective effect against various toxic agents by its antioxidant action in liver tissues. Thus, PG may be used in prevention and treatment of drug-induced liver cell injury. However, the precise mechanisms of PG protection remain to be determined.

• Journal of Society of Preventive Korean Medicine
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• v.4 no.2
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• pp.170-192
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• 2000

Objectives : This study was carried out to research antioxidant effects of Sagunja-Tang(SA) through in vitro and vivo experiments, and tried to investigate the relation between oxidation of tissues and deficiency of Qi. Methods and results : HPLC analysis of glycyrrhizine - known to be the main compound of Radix Glycyrrhizae - was done to certify the quality of SA. Chemiluminescence was initiated by adding tort-butyl hydroperoxide (t-BHP) to rabbit polymorphonuclear leukocytes (neutrophils), and generated reactive oxygen species (superoxide anion) decreased significantly by SA as dose dependent manner. Cell injury during 60 minutes tissue incubation was initiated by adding t-BHP, a hydrophobic hydroperoxide and $H_2O_2$, an water soluble oxidant to rat renal cortical and liver slices. Percentage cell death and lipid peroxidation were estimated by measuring lactate dehydrogenase (LDH) and malondialdehyde (MDA), a product of lipid peroxidation. t-BHP induced % cell death of renal cortical slices and lipid peroxidation of renal cortical and liver slices were decreased significantly by SA. SA decreased significantly % cell death and lipid peroxidation of renal cortical and liver slices induced by $H_2O_2$, too. Acute renal and liver injury induced by $HgCl_2\;and\;CCl_4$, which initiated from free radical, were applied to mice and metabolic data were obtained. Data showed protective effects of SA on acute renal injury caused by decrease of glomerular filtration. SA protected acute liver injury too. Conclusions Through this study, we found that SA have antioxidant effects and tissue oxidation was similar to deficiency of Qi. And further studies have to be followed to certify the mechanisms.

• Korean Journal of Acupuncture
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• v.22 no.1
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• pp.117-132
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• 2005

Objectives : This study was carried out to determine whether Juglandis Semen herbal acupuncture (JSA) exerts the protective effect against toxic agent-induced live. cell damage. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring maiondialdehyde (MDA), a product of lipid peroxidation, in rabbit liver slices. Results : When tissues were incubated with 0.5 mM Hg for $10{\sim}120\;min$, LDH release and lipid peroxidation were increased as a function of incubation time, and these effects were significantly prevented by addition of 0.1% JSA. Hg increased LDH release and lipid peroxidation in dose-dependent manner over the range of $0.1{\sim}l\;mM$ concentrations, which were reduced by 0.1% JSA. When tissues were treated with 0.5 mM Hg in the presence of $0.05{\sim}l\;%$ JSA, LDH release and lipid peroxidation induced by Hg were prevented by JSA in a dose-dependent fashion. JSA at 0.5 and 1% prevented completely effects of 0.5 mM Hg. When tissues were treated with 0.5 mM Hg for 60 min, LDH release and lipid peroxidation were increased, which were significantly prevented by addition of 0.1 % JSA. tert-Butyl hydroperoxide (tBHP) increased LDH release and lipid peroxidation, which were significantly reduced by 0.1 % JSA. Such protective effects were similar to those of N,N'-diphenyl-p-phenylenediamine (DPPD), a potent antioxidant. When tissues were treated with 0.5 mM Hg, activities of catalase and glutathione peroxidase were inhibited, and glutathione content was also reduced. Such effects were prevented by JSA, but not by DPPD. JSA prevented Hg-induced morphological changes. Conclusions : These results indicate that JSA exerts the protective effect against liver cell injury induced by toxic agents through antioxidant action, and this effect may be attributed to an increase in activities of endogeous anitoxidant enzymes and GSH content. However, antioxidant effect of JSA is different from that of a well-known potent antioxidant DPPD.