Mi-Jeong Kim

The Antioxidant Effect of Hot Water Extract from the Dried Radish (Raphanus sativus L.) with Pressurized Roasting

The antiradical property of hot water extract from dried radish (DR) or dried radish roasted with pressure (DRRP) was investigated in vitro and in LLC-PK1 cell system. The contents of total free amino acid and reducing sugar in DR were decreased by 72.86% and 3.17%, respectively, after pressurized roasting. In vitro test, for DR and DRRP for DPPH radical scavenging activity were 646.70 and , 896.10 and for superoxide anion radical, and 722.26 and for hydroxy radical, respectively. The radical scavenging effects of DRRP was significantly greater than those for DR (p at which oxidative stresses were induced by superoxide, nitric oxide and peroxynitrite generated in the treatment of pyrogallol, SNP, and SIN-1, respectively. Cell viability was increased in the presence of DR or DRRP, dose dependently (p were greater than those of DR at the same concentration tested (p

Bamboo Culm Extract Supplementation Elevates HDL-Cholesterol and Ameliorates Oxidative Stress in C57BL/6 Mice Fed Atherogenic Diet

Previously, we reported that bamboo culms possess a stronger antioxidative capacity than bamboo leaves in vitro. In this study, we investigated whether bamboo culm extract (BCE) supplementation ameliorates oxidative stress and hepatic nuclear factor kappaB (NF kappa B) activation in C57BL/6 mice fed an atherogenic diet. In addition, the effect of BCE supplementation on plasma lipid levels of the animals was tested. The mice were randomly assigned to a normal diet, an atherogenic diet (control), or an atherogenic diet supplemented with 1% (wt/wt) BCE or 3% (wt/wt) BCE for 16 weeks. Atherogenic diet-induced oxidative stress, measured by hepatic thiobarbituric acid-reactive substances and protein carbonyls, was significantly lower in the BCE-supplemented groups than in the control (P < .05). Total antioxidative capacity was elevated in the BCE groups, along with greater activities of antioxidative enzymes such as superoxide dismutase and catalase, compared to the control or normal groups (P < .05). The hepatic NF kappa B binding activities were significantly lower in the BCE groups as well (P < .05). The high-density lipoprotein-cholesterol level was significantly elevated by BCE supplementation (P < .05), whereas the effects of BCE on triglyceride and total cholesterol were inconsistent. Results from this study suggest that BCE supplementation may lessen oxidative stress via a series of changes, including a reinforced antioxidant system, and also suggest that the lowered oxidative stress status may down-regulate the activation of inflammatory mediators.

Chondroitin Sulfate-Rich Extract of Skate Cartilage Attenuates Lipopolysaccharide-Induced Liver Damage in Mice

The protective effects of a chondroitin sulfate-rich extract (CSE) from skate cartilage against lipopolysaccharide (LPS)-induced hepatic damage were investigated, and its mechanism of action was compared with that of chondroitin sulfate (CS) from shark cartilage. ICR mice were orally administrated 200 mg/kg body weight (BW) of CS or 400 mg/kg BW of CSE for 3 consecutive days, followed by a one-time intraperitoneal injection of LPS (20 mg/kg BW). The experimental groups were vehicle treatment without LPS injection (NC group), vehicle treatment with LPS injection (LPS group), CS pretreatment with LPS injection (CS group), and CSE pretreatment with LPS injection (CSE group). Hepatic antioxidant enzyme expression levels in the CS and CSE groups were increased relative to those in the LPS group. In LPS-insulted hepatic tissue, inflammatory factors were augmented relative to those in the NC group, but were significantly suppressed by pretreatment with CS or CSE. Moreover, CS and CSE alleviated the LPS-induced apoptotic factors and mitogen-activated protein kinase (MAPK). In addition, CS and CSE effectively decreased the serum lipid concentrations and downregulated hepatic sterol regulatory element-binding proteins expression. In conclusion, the skate CSE could protect against LPS-induced hepatic dyslipidemia, oxidative stress, inflammation, and apoptosis, probably through the regulation of MAPK signaling.