• Clinical and Experimental Pediatrics
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• v.51 no.10
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• pp.1102-1111
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• 2008

Purpose : Resveratrol, extracted from red wine and grapes, has an anti-cancer effect, an antiinflammatory effect, and an antioxidative effect mainly in heart disease and also has neuroprotective effects in the adult animal model. No studies for neuroprotective effects during the neonatal periods have been reported. Therefore, we studied the neuroprotective effect of resveratrol on hypoxic-ischemic brain damage in neonatal rats via anti-apoptosis. Methods : Embryonic cortical neuronal cell culture of rat brain was performed using pregnant Sprague-Dawley (SD) rats at 18 days of gestation (E18) for the in vitro approach. We injured the cells with hypoxia and administered resveratrol (1, 10, and $30{\mu}g/mL$) to the cells at 30 minutes before hypoxic insults. In addition, unilateral carotid artery ligation with hypoxia was induced in 7-day-old neonatal rats for the in vivo approach. We injected resveratrol (30 mg/kg) intraperitoneally into animal models. Real-time PCR and Western blotting were performed to identify the neuroprotective effects of resveratrol through anti-apoptosis. Results : In the in vitro approach of hypoxia, the expression of Bax, caspase-3, and the ratio of Bax/Bcl-2, indicators of the level of apoptosis, were significantly increased in the hypoxia group compared to the normoxia group. In the case of the resveratrol-treated group, expression was significantly decreased compared to the hypoxia group. And the results in the in vivo approach were the same as in the in vitro approach. Conclusion : The present study demonstrates that resveratrol plays neuroprotective role in hypoxic-ischemic brain damage during neonatal periods through the mechanism of anti-apoptosis.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.9
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• pp.1185-1193
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• 2006

This study investigated the effects of green tea on the disorders of lipid metabolism, oxidative system and hepatic functions induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), using adult male rats (SD) for 3 weeks. These 36 animals were divided into four groups. TCDD ($50{\mu}g/kg$ BW) was intraperitoneally injected at the beginning of experiment. Green tea powder was added 1% or 3% levels in basal diets respectively. Relative weights of thymus were decreased about one-third of control group, but those of liver, brain and testis were significantly increased in rats treated TCDD. Neutrophill% and lymphocyte% by TCDD treatment was improved by green tea diets. In liver functional enzyme, elevation of glutamic oxaloacetic transaminase (GOT) and alkaline phosphatase (ALP) activities due to TCDD treatment was lowered by green tea diets. The concentrations of serum and liver lipids were significantly increased by TCDD treatment, however, those of serum and liver triglyceride tended to decrease by green tea diets. Fecal lipid excretion was increased in rats fed green tea diets. Especially, fecal total cholesterol level was significantly elevated by 3% green tea diets. The activities of superoxide dismutase (SOD) were increased in rats fed 3% green tea diets. Increment of benzphetamine N-demethylase (BPND) activity by TCDD treatment was declined by 1% green tea diets. These results indicate that green tea can exert improving effects on liver lipid accumulation and unfavorable hepatic functions, and elevate antioxidation.

• Journal of Ginseng Research
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• v.32 no.4
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• pp.382-389
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• 2008

To achieve a better understanding of protective effects of water extracts of Panax ginseng against TCDD-induced toxicities, we monitored physiological and clinical changes in rat for 4 weeks after administrations of each Panax Ginseng extract or TCDD, and co-administration of the two materials. For this study, 120 male Sprague-Dawley (SD) rats weighing 190-210 g each (8 weeks old) were divided into four groups: TCDD-administered, co-administered group with TCDD and ginseng extract, ginseng extract-administered, and control group. The TCDD-administered group received single dose of TCDD in a corn oil vehicle ($25\;{\mu}g/kg$ body weight) by intraperitoneal administration on Day 1. The Panax ginseng extracts-administered group received intraperitoneally 100 mg/kg body weight every other day for one month. For the co-administered group with TCDD and ginseng extracts, Panax ginseng extracts were intraperitoneally administered to rats at 100 mg/kg body weight every other day for one month after a single intraperitoneal dose of $25\;{\mu}g$ of TCDD/kg body weight on Day 1. Panax ginseng extracts attenuated the mortality induced by TCDD administration. The extracts also slightly attenuated the TCDD-induced body weight loss. Administration of TCDD alone increased liver weight at 2, 5, and 16 days after administration of TCDD. Administration of Panax ginseng extracts rather decreased liver weight through whole the experimental period, but which was statistically insignificant. Administration of TCDD alone at $25\;{\mu}g/kg$ body weight increased both serum enzyme activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) at 32 days, indicating that liver damage occurred maximally at that time. Ginseng extract administration caused insignificant changes in serum ALT, but gradually decreased in AST as the exposure time increased. Coadministration of TCDD and ginseng extracts caused serum AST activity to significant recovery to normal value at 16 days and 32 days after exposure to TCDD. The extracts also significantly decreased the TCDD-induced ALT activity after 16 days of TCDD administration. These results suggest that Panax ginseng extracts may possess a protective effect against TCDD-induced toxicities including hepatotoxicity in rats.