• Toxicological Research
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• v.18 no.3
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• pp.293-300
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• 2002

Chemical carcinogen-induced alteration of aldehyde metabolic enzymes were examined in clone 9 cell. Diethylnitrosamine (DENA), N-nitrosoethylurea (NEU) and N-nitrosomorpholine (NNM) were wed as model carcinogens. Changes in enzyme activities by repetitive treatment of DENA, NEU or NNM were analyzed in terms of specific activities and activity stainings of the enzymes on the gel. Upon treatment of DENA, lipid peroxide level increased upto 10 fold, indicating strong oxidative stress state of the cell. Notable enhancement of ADH and ALDH activity occurred after DENA treatment, while glutathione-S-transferase activity was slightly increased. Furthermore, about 2.5 fold higher superoxide dismutase (SOD) activity was detected during deactivation of catalase (CAT) activity by repetitive treatment of DENA. However in NEU-treated cell, about 2.3 fold higher ALDH activity was found while ADH activity was slightly increased. Notable increase CAT and SOD could also be found. In contrast, maximum 3.5 fold higher CAT activity occurred during SOD deactivation in NNM-treated cell. These results suggest that there might be different enzymatic responses in relation to cell protection against DENA, NEU or NNM.

• Toxicological Research
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• v.11 no.2
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• pp.181-185
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• 1995

To know the mechanism of biphenyl dimethyl dicarboxylate (DDB) in the protection of chemically induced hepatotoxicity, the activity of glutamic pyruvic tran.saminase (GPT) and the level of lipid peroxidation metabolite (malondialdehyde, MDA) and ATP content in hepatocytes were determined in serum and primarily cultured hepatocytes. For in vibo study, rats were pretreated with DDB (300 mg/ kg, p.o.)for 7 days. DDB pretreatment efficiently reduced the elevation of serum GPT activity induced by carbon tetrachloride (1.6 ml/kg, s.c.) and acetaminophen administration (1500 mg/kg, i.p.). In ex vivo study, hepatocytes were isolated from the rats pretreated with DDB (300 mg/kg, p.o.)for 7 days and cultured for 12 hrs before inducing cytotoxicity with chemicals. The MDA formation and the GPT release induced by adriamycin $(1\times10^{-4} mg/ml)$ and cisplatin $(2\times10^{-4} mg/ml)$ were markedly decreased in the hepatocytes from the rats pretreated with DDB as compared to vehicle only. However, DDB pretreatment did not prevent the decrease of ATP contents of hepatocytes induced by cisplatin and adriamycin. In in vitro experiment, DDB was pretreated in primary cultured hepatocytes for 3 days. DDB enhanced the decreases of ATP contents induced by cisplatin and adriamycln. These results suggest that DDB may protect the hepatocytes from injury induced by hepatotoxlcants through inhibiting the lipid peroxidation.

• Advances in Traditional Medicine
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• v.3 no.4
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• pp.205-211
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• 2003

Stem bark of Cinchona sp. (Rubiaceae) is one of the well known drugs for its therapeutic values in traditional as well as modern medicine. Even though a lot of work has been carried out on quinoline alkaloids of Cinchona, its phenolic constituents received very little attention. In the present study, we evaluated antioxidant properties of C. officinalis stem bark methanolic extract and water extract containing phenolic compounds (total phenolics 21.37, 5.18% w/w respectively in the two extracts) in different in vitro and ex vivo models viz., antiradical activity by DPPH reduction, superoxide radical scavenging activity in riboflavin/light/NBT system, nitric oxide radical scavenging activity in sodium nitroprusside/Greiss reagent system and inhibition of lipid peroxidation induced by iron-ADP-ascorbate in liver homogenate and haemolysis of erythrocytes induced by phenylhydrazine in erythrocyte membrane stabilization study. Both the extracts exhibited very good antioxidant activity in all the models tested. The phenolic compounds including tannins present in the stem bark seem to offer protection from the oxidative damage.

• YAKHAK HOEJI
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• v.44 no.3
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• pp.237-244
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• 2000

Liver isolated from 18 hours fasted rats was subjected to $N_2$hypoxia (for 45 min) followed by reoxygenation (for 30 min). The perfusion medium used was Krebs-Henseleit bicarbonate buffer (pH 7.4, $37^{\circ}C$). Vitamin C (0.5 mM) and trolox C (0.5 mM), soluble vitamin E analog, were added to perfusate. Lactate dehydrogenase (LDH), total glutathione, oxidized glutathione, lipid peroxide and drug-metabolizing enzymes were measured. After hypoxia LDH significantly increased but this increase was attenuated by vitamin C and combination of vitamin C and E. Total glutathione and oxidized glutathione in perfusate markedly increased during hypoxia and this increase was inhibited by vitamins C, E and its combination. Similarly; oxidized glutathione and lipid peroxide in liver tissue increased after hypoxia and reoxygenation and this increase was inhibited by vitamin I and combination of vitamin C and E. Hepatic drug metabolizing function (phase I, II) were suppressed during hypoxia but improved during reoxygenation. While vitamins C and E only increased glucuronidation, the combination of vitamin C and E increased the oxidation, glucuronidation and sulfation. Our findings suggest that vitamins C and E synergistically ameliorates hepatocellular damage as indicated by abnormalities in drug metabolizing function during hypoxia/reoxygenation and that this protection is in major part, caused by decreased oxidative stress.

• The Korea Journal of Herbology
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• v.21 no.3
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• pp.69-74
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• 2006

Objectives : This study was undertaken to determine if a combined(SPe) has a protective effect against functional failure induced by $CCl_4$ in rat liver. Methods : Acute liver injury which initiated from free radical induced by $CCl_4$, were applied to rats and data were obtained. Liver injury was estimated by measuring aspartate aminotransferase(AST) and alanine aminotransferase(ALT) activity in serum. Lipid peroxidation was examined by measuring malondialdehyde, a product of lipid peroxidation. GSH activities in liver tissues were also measured. Results : When rats were treated intraperitoneally with $CCl_4$, serum AST and ALT were increased compared with the control, which was significantly inhibited by pretreatment of SPe. SPe also prevented reduction in GSH induced by $CCl_4$. Conclusion : Above results suggest that SPe exerts protective effect against $CCl_4$ by its antioxidant action in liver tissues. Thus, SPe may be used in prevention and treatment of drug-induced liver cell injury. However, the precise mechanisms of SPe protection remain to be determined.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.47-54
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• 2014

The present study was aimed to evaluate the antioxidant defense system of cinnamaldehyde in normal, diabetic rats and its possible protection of pancreatic ${\beta}$-cells against its gradual loss under diabetic conditions. In vitro free radical scavenging effect of cinnamaldehyde was determined using DPPH (1,1-diphenyl-2-dipicrylhydrazyl), superoxide radical, and nitric oxide radical. Streptozotocin (STZ) diabetic rats were orally administered with cinnamaldehyde at concentrations of 5, 10 and 20 mg/kg body weight for 45 days. At the end of the experiment, the levels of plasma lipid peroxides and antioxidants such as vitamin C, vitamin E, ceruloplasmin, catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase were determined. A significant increase in the levels of plasma glucose, vitamin E, ceruloplasmin, and lipid peroxides and significant decrease in the levels of plasma insulin and reduced glutathione were observed in the diabetic rats. Also the activities of pancreatic antioxidant enzymes were altered in the STZ-induced diabetic rats. The altered enzyme activities were reverted to near-normal levels after treatment with cinnamaldehyde and glibenclamide. Histopathological studies also revealed a protective effect of cinnamaldehyde on pancreatic ${\beta}$-cells. Cinnamaldehyde enhances the antioxidant defense against reactive oxygen species produced under hyperglycemic conditions and thus protects pancreatic ${\beta}$-cells against their loss and exhibits antidiabetic properties.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.162-162
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• 1998

Various natural compounds act as antioxidants in protection against lipid peroxidation. Lipid peroxidation yields a variety of decomposition products which have been implicated in not only decreasing the nutritional value of food, but also in developing an off-flavor and toxic substances. As a source of safer and more effective natural antioxidants of natural origin have been widely investigated. Some Indonesian plants have evaluated for their antioxidative activity, and suggested the possible existence of various antioxygenic compounds in them. We attempted to study such antioxygenic compounds with simple method evaluation. As we are interested in the natural product compounds, we examined of several sample such as edible sea-weeds, and some edible fruits. Sea-weed, Eisenia bicyclis, one of the edible brown algae, exhibited the activity. As a traditional food additive consumed by Indonesian, Garcinia parvifolia is used as taste supplement in region West Sumatra, have been studied. Our current studies on the semi-polar fractions shows the activity by the thiocyanate method test. Another sample, Garcinia mangostana, a famous fruit with sweet taste, the part kernel have also evaluated. The acidic fraction of the extract showed antioxidative activity. Some other active components were found in the neutral and BuOH fractions.

• The Korean Journal of Food And Nutrition
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• v.29 no.3
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• pp.307-312
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• 2016

This study was performed to investigate the effects of Acer tegmentosum Maxim. extract (ATE) on non-alcoholic fatty liver in Sprague Dawley (SD) rats. During oral administration of ATE, non-alcoholic fatty liver was induced by treatment with DL-ethionine. The lipid, total cholesterol (T-CHO) and malondialdehyde (MDA) in the liver tissue of ATE-fed rats showed lower levels, as compared to ATE-unfed rats. In ATE-fed rats, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and ${\gamma}$-glutamyl transferase (GGT) were lower than the case of ATE-unfed rats. Oil red staining of the liver showed that the lipid deposits were decreased by feeding ATE. These results strongly indicated that ATE has positive effects of protection against non-alcoholic fatty liver formation.

• The Journal of Korean Medicine
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• v.26 no.1 s.61
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• pp.76-84
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• 2005

Objective: The purpose of this study was to examine the protective efficacy of GHT on alcoholic liver injury. Methods: We measured the rate of alcohol oxidation, serum level of liver enzyme, lipid peroxidation level in liver tissue, and inflammatory related cytokine expressions in the liver. Results : GHT showed liver protective effects, lowered the levels of AST and LDH in serum and inhibited lipid peroxidation in liver tissue, and enhanced alcohol oxidation. GHT treatment up-regulated IL-10 in the liver, whereas it down­regulated $TNF-\alpha,\;TGF-\beta$, and Fas ligand. Conclusion : From these results, GHT is presumed to work in the liver in protective roles not through the pathway of alcohol metabolism but mainly by anti-inflammation activity in our model.

• Journal of Ginseng Research
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• v.38 no.3
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• pp.161-166
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• 2014

Ginseng is widely used for its promising healing and restorative properties as well as for its possible tonic effect in traditional medicine. Nowadays, many studies focus on purified individual ginsenoside, an important constituent in ginseng, and study its specific mechanism of action instead of whole-plant extracts on cardiovascular diseases (CVDs). Of the various ginsenosides, purified ginsenosides such as Rb1, Rg1, Rg3, Rh1, Re, and Rd are the most frequently studied. Although there are many reports on the molecular mechanisms and medical applications of ginsenosides in the treatment of CVDs, many concerns exist in their application. This review discusses current works on the countless pharmacological functions and the potential benefits of ginseng in the area of CVDs. Results: Both in vitro and in vivo results indicate that ginseng has potentially positive effects on heart disease through its various properties including antioxidation, reduced platelet adhesion, vasomotor regulation, improving lipid profiles, and influencing various ion channels. To date, approximately 40 ginsenosides have been identified, and each has a different mechanism of action owing to the differences in chemical structure. This review aims to present comprehensive information on the traditional uses, phytochemistry, and pharmacology of ginseng, especially in the control of hypertension and cardiovascular function. In addition, the review also provides an insight into the opportunities for future research and development on the biological activities of ginseng.