• YAKHAK HOEJI
• /
• v.50 no.3
• /
• pp.191-198
• /
• 2006

Acanthopanax species have traditionally been used as a tonic, a sedative as well as in the treatment of rheumatism, hypertension and diabetes. In the present study, oxidative stress was induced in Vero cells by incubating the cells with glucose and the cell viability was measured by MTT assay. The concentration of glucose which 50% of cell viability was 125 mM $(IC_{50})$ and the cell viability was increased to $87.6{\pm}8.8%$ by treatment of the extracts of Acanthopanax divaricatus var. albeofructus. The antioxidative activity of water extract of different parts of the Acanthopanax plant was investigated by DPPH (1,1-diphenyl-2-picrylhydrazyl) assay, xylenol orange assay, TBARS (thiobarbituric acid reactive substances) assay and enzyme (superoxide anion and catalase) assay. Each extract (leaves, root, stem and fruits) of the plant showed free radical and $H_2O_2$ scavenging activity. The extract also inhibited lipid peroxidation and recovered enzyme (superoxide anion dismutase and catalase) activity in Vero cells treated with glucose.

• Journal of Sericultural and Entomological Science
• /
• v.42 no.1
• /
• pp.58-64
• /
• 2000

This study was designed to investigate the effects of silk fibroin powder (Mw 500) on oxidative stress and membrane fluidity in liver membranes of rats. Sprague-Dawley (SD) male rats (160$\pm$10g) were fed basic diet (control group), and experimental diets (SEP-2.5 and SFP-5.0 groups) added 2.5 and 5.0 g/kg BW/day for 6 weeks. Cholesterol levels resulted in a significant decrease (12.1% and 9.0%, respectively) in the liver mitochondria and microsomes of SEP-5.0 group compared with control group. Membrane fluidity as significantly increased (16.1% and 16.5%, 5.8% and 17.4%) in the liver mitochondria and microsomes were significantly inhibited (16.1% and 18.3%, 8.1% and 15.1%, respectively) at the SFP-2.5 and SEP-5.0 groups compared with control group. Induced oxygen radicals (BOR) in liver mitochondria and microsomes were significantly inhibited (16.1% and 18.3%, 8.1% and 15.1%, respectively) at the SFP-2.5 and SEP-5.0 groups compared with control group. Induced oxygen radicals (IOR) in liver microsomes were significantly inhibited (17.0% and 26.6%, respectively) at the SFP-2.5 and SFP-5.0 groups compared with control group, but IOR in liver mitochondria was significantly inhibited about 12.3% at the SWP-400 group only compared with control group. Lipid peroxide (LPO) levels were significantly decreased (8.3% and 18.0%, 13.4% and 18.4%, respectively) in the liver mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. Oxidized protein (OP) levels were dose-dependently decreased (5.4% and 11.6%, 19.0% and 24.4%, respaectively) in the iver mitochondria and microsomes of SFP-2.5 and SFP-5.0 groups compared with control group. These results suggest that administration of SFP may play an effective role in attenuating an oxidative stress and increasing a membrane fluidity in liver membranes.

• Journal of Ginseng Research
• /
• v.36 no.3
• /
• pp.248-255
• /
• 2012

Potential antioxidant effect of processed ginseng (sun ginseng, SG) on oxidative stress generated by tert-butyl hydroperoxide (t-BHP) was investigated in HepG2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) leakage test demonstrated that SG dose-dependently prevents a loss of cell viability against t-BHP-induced oxidative stress. Also, SG treatment dose-dependently relieved the increment of activities of hepatic enzymes, such as aspartate aminotrasferase and alanine aminotransferase, and lipid peroxidation mediated by t-BHP treatment in HepG2 cells. SG increased the gene expression of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. However, high dose of SG treatment caused decrease in mRNA level of glutathione peroxidase as compared to low dosage of SG-treated cells. The gene expression of glutathione reductase was found to be slightly increased by SG treatment. In addition, SG extract attributed its hepaprotective effect by inducing the mRNA level of bcl-2 and bcl-xL but reducing that of bax. But, the gene expression of bad showed no significant change in SG-treated HepG2 cells. These findings suggest that SG has hepatoprotective effect by showing reduction of LDH release, activities of hepatic enzymes and lipid peroxidation and regulating the gene expression of antioxidant enzymes and apoptosis-related molecules against oxdative stress caused by t-BHP in HepG2 cells.

• The Korean Journal of Physiology and Pharmacology
• /
• v.10 no.2
• /
• pp.79-83
• /
• 2006

We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.