• Korean Journal of Food Science and Technology
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• v.44 no.5
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• pp.643-647
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• 2012

The antioxidant capacity of aloe vera gel (AG), aloe vera exudates (AE), and a low molecular filtrate of aloe vera gel (ALMF) prepared from aloe vera grown on Jeju Island, Korea was evaluated using 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2'-azinobis-3-ethyl-benzothiazoline-6-sulfonic acid (ABTS), and oxygen radical absorbance capacity (ORAC) assays, and total phenolic content (TPC), and total flavonoid content (TFC) were determined. The phenolic compounds in aloe samples were analyzed. Antioxidant capacities in oil-in-water emulsions following riboflavin photosensitization were analyzed using lipid hydroperoxide. AE had significantly higher antioxidant capacity than that of the other samples based on the DPPH, ABTS, and ORAC assays (p<0.05). Lipid hydroperoxide values of 5 mg/mL for AG, AE, and ALMF were 521.78, 272.32, and 699.89 mmol/kg oil, respectively, whereas that of samples without aloe vera was 893.07 mmol/kg oil over 48 h. AE had higher TPC and TFC values. Aloesin and aloin were found in AE, whereas those compounds were only found in trace amounts in AG and ALMF.

• Nutrition Research and Practice
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• v.7 no.6
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• pp.475-480
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• 2013

The purpose of this study was to determine the antioxidant effect of fucoxanthin. After rats were fed a normal fat diet (NF), high fat diet (HF), and high fat with 0.2% fucoxanthin diet (HF + Fxn) for 4 weeks, the markers of oxidative stress and antioxidant capacity like lipid peroxidation, plasma total antioxidant capacity (TAC), and activities of antioxidant enzymes (catalase, superoxide dismutase (SOD), and gluthathione peroxidase (GSH-Px)) were determined. mRNA expression of transcription factor, nuclear erythroid factor like 2 (Nrf2), and its target genes such as NAD(P)H quinone oxidoreductase1 (NQO1) and heme oxygenase-1 (HO-1) were also determined. Mean weight gain in the HF + Fxn group was lower, without statistical significance, and the total food intake in the HF + Fxn group was lower than that in the HF group (P < 0.05). The activity of GSH-Px (P < 0.05) in plasma was significantly higher in the HF + Fxn group than those in the HF group (P < 0.05). In the liver, the activities of catalase (P < 0.05) and GSH-Px (P < 0.05) in the HF + Fxn group were significantly higher than those in the HF group. Plasma TAC level was significantly higher in the HF + Fxn group than that in the HF group (P < 0.05). Lipid peroxidation in plasma tended to be lower without statistical significance. Fucoxanthin supplements were shown to have higher mRNA expression of Nrf2 and NQO1 than those in the high fat diet only group (P < 0.05). In conclusion, supplementation of fucoxanthin improved the antioxidant capacity, depleted by high fat diet, by activating the Nrf2 pathway and its downstream target gene NQO1. Therefore, supplementation of fucoxanthin, especially for those who consume high fat in their diet, may benefit from reduced risk of oxidative stress.

• Korean Journal of Acupuncture
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• v.26 no.2
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• pp.109-126
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• 2009

Objectives: To investigate the effects of Chrysanthemum indicum L. pharmacopuncture on lipids, antioxidant capacity and anti-inflammation in rats fed high-fat diet. Methods: Hyperlipidemic rats induced by high-fat diet were divided into 5 groups: no treatment control (normal, n=8), high-fat diet only control (control, n=8), high-fat diet and Chrysanthemum indicum L. pharmacopuncture at CV4 group (TI, n=8), high-fat diet and Chrysanthemum indicum L. pharmacopuncture at CV17 group (TII, n=8), and high-fat diet and Chrysanthemum indicum L. pharmacopuncture at EX-HN3 group (TIII, n=8). They were given pharmacopuncture accordingly every other day for two weeks followed by analyses of lowering lipids effects, oxidative capacity and anti-inflammatory effects. Results: Compared with the control, pharmacopuncture groups showed significantly decreased plasma total cholesterol (TC), liver thiobarbituric acid reactive substance (TBARS), catalase, glutathione peroxidase, neutrophils, monocytes, plasma and liver IL-$1{\beta}$, and plasma and liver IL-6. In other parameters including plasma and liver triglyceride, liver TC, LDL-cholesterol, HDL-cholesterol, liver TBARS, supraoxide dismutase, total protein, albumin, blood cell analysis, plasma and liver TNF-$\alpha$, and IL-10, there was no significant difference between control and pharmacopuncture groups. No clear acupoint-specificity was observed. Conclusions: Chrysanthemum indicum L. pharmacopuncture may improve control of hyperlipidemia.

• Toxicological Research
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• v.31 no.2
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• pp.191-201
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• 2015

We evaluated the inhibitory effect of Pueraria lobata root ethanol extract (PLREE) on lipid accumulation during 3T3-L1 differentiation to adipocytes by measuring the intracellular expression of adipogenic, lipogenic, and lipolytic markers and lipid accumulation. The total polyphenol and flavonoid content of PLREE were 47 and 29 mg/g, respectively. The electron donating capacity of PLREE at $1,000{\mu}g/mL$ was 48.8%. Treatment of 3T3-L1 preadipocytes with 100, 250, or $500{\mu}g/mL$ PLREE for 8 days dose-dependently promoted the differentiation of 3T3-L1 cells. In contrast, the lipid content of PLREE-treated cells was significantly reduced by 7.8% (p < 0.05), 35.6% (p < 0.001), and 42.2% (p < 0.001) following treatment with 100, 250, and $500{\mu}g/mL$ PLREE, respectively, as compared to differentiated control cells. PLREE upregulated peroxisome proliferator-activated receptor ${\gamma}$ mRNA and protein, and sterol regulator element-binding protein-1c mRNA levels, but did not affect CCAAT/enhancer binding-protein ${\beta}$ and ${\alpha}$ mRNA levels. PLREE also downregulated acetyl-CoA carboxylase mRNA and protein, fatty acid synthase (FAS) protein, and leptin mRNA levels, but did not affect FAS mRNA expression. PLREE upregulated adipose triglyceride lipase mRNA and protein expression, and hormone-sensitive lipase (HSL) protein expression, but did not affect HSL mRNA expression. In conclusion, we found that PLREE enhanced adipogenesis, but reduced lipogenesis, resulting in decreased lipid accumulation in 3T3-L1 cells.

• Korean Journal of Plant Resources
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• v.19 no.6
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• pp.649-654
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• 2006

The objective of present study was to investigate the anti oxidative and hepatoprotective effects of tomato extracts. Total antioxidant capacity and total antioxidant response were 5.5 and $19.8{\mu}g$ Trolox equivalent per mg of tomato extract, respectively. DPPH radical scavenging activity of tomato extracts ($10mg\;ml^{-1}$) was 70% as compared to 100% by pyrogallol solution as a reference. The effect of the tomato extracts on lipid peroxidation was examined using rat liver mitochondria induced by iron/ascorbate. Tomato extracts at the concentration of $0.5mg\;ml^{-1}$ significantly decreased TBARS concentration. Tomato extracts prevented lipid peroxidation in a dose-dependent manner. The effect of the tomato extracts on reactive oxygen species (ROS) generation was examined using cell-free system induced by $H_2O_2/FeSO_4$. Addition of $1mg\;ml^{-1}$ of tomato extracts significantly reduced dichlorofluorescein (DCF) fluorescence. Tomato extracts caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that tomato extracts significantly prevented ROS generation in vitro. The effect of tomato extracts on cell viability and proliferation was examined using hepatocyte culture. Primary cultures of rat hepatocytes were incubated with 1mM tert-butyl hydroperoxide (t-BHP) for 90 min in the presence or absence of tomato extracts. MTT values by addition of tomato extracts at the concentration of 2, 10, and $20mg\;ml^{-1}$ in the presence of t-BHP were 13, 33 and 48%, respectively, compared to 100% as control. Tomato extracts increased cell viability in a dose-dependent manner. These results demonstrate that tomato extracts suppressed lipid peroxidation and t-BHP-induced hepatotoxicity and scavenged ROS generation. Thus antioxidant and hepatoprotective effects of tomato extracts seem to be due to, at least in part, the prevention from free radicals-induced oxidation, followed by inhibition of lipid peroxidation.

• The Journal of Korean Medicine
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• v.28 no.1 s.69
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• pp.137-147
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• 2007

Objective : The objective of this study was to investigate the antioxidative effects of Carthami Flos extract. Methods : Total antioxidant status was examined by total antioxidant capacity(TAC) and total antioxidant response(TAR) against potent free radical reactions. The effect of Carthami Flos extract was examined far details of total phenolic content concentration at which 1,1-dipheny1-2-picrylhydrazyl(DPPH) radical scavenging activity was inhibited, the inhibitory effect on lipid peroxidation, and the effect on reactive oxygen species(ROS) generation. Results : TAC of Carthami Flos extract at the concentration of 5 mg/ml was 1.84 mM Trolox equivalent. 2. TAR of Carthami Flos extract, on the other hand, couldn't be determined due to interference from unidentified compounds. 3. Total phenolic content of Carthami Flos extract at the concentration of 5 mg/ml was 2.01 mM gallic acid equivalent. 4. Concentration of Carthami Flos extract at which DPPH radical scavenging activity was inhibited by 50% was 6.43 mg/ml as compared to 100% by Pyrogallol solution as a reference. 5. The inhibitory effect of the extract on lipid peroxidation was examined using rat liver mitochondria induced by FeS04/ascorbic acid. Carthami Flos extract at the concentration of 10 ms/ml slightly but significantly decreased TBARS concentration. The extract continued to prevent lipid peroxidation in a dose-dependent manner. 6. The effect of Carthami Flos extract on reactive oxygen species(ROS) generation was examined using a cell-free system induced by hydrogen peroxide/FeS04. Addition of 1 mg/ml of Carthami Flos extract significantly reduced dichlorofluorescein(DCF) fluorescence. Carthami Flos extract caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that the ektract significantly prevented ROS generation in vitro. Conclusion: : Antioxidant efffcts of Carffami ffor extract seem to be due, at least in part, to the prevention offree radical-induced oxidation, fellowed by inhibition of lipid peroxidation.

• The Journal of Korean Medicine
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• v.28 no.1 s.69
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• pp.148-158
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• 2007

Objective : The objective of this study was to investigate the antioxidant effects of Mori Folium extract. Methods Total antioxidant status was examined by total antioxidant capacity(TAC) and total antioxidant response(TAR) against potent free radical reactions. The effect of Mori Folium extract was examined by measuring total phenolic content, concentration at which 1,1-dipheny1-2-picrylhydrazyl(DPPH) radical scavenging activity was inhibited, inhibitory effect on lipid peroxidation, and the effect on reactive oxygen species(ROS) generation. Results : 1. TAC and TAR of Mori Folium extract at the concentration of 5 mg/ml were 1.61 and 1.24 mM Trolox equivalents, respectively. 2. Total phenolic content of Mori Folium extract at the concentration of 5 mg/Ml was 1.70 mM gallic acid equivalent. 3. Concentration of Mori Folium extract at which DPPH radical scavenging activity was inhibited by 50% was 2.29 m9/m4 as compared to 100% by Pyrogallol solution as a reference. 4. The inhibitory effect of the extract on lipid peroxidation was examined using rat liver mitochondria induced by FeSO$_4$/ascorbic acid. Mori Folium extract at the concentration of 10 mg/ml significantly decreased thiobarbituric acid reactive substances(TBARS) concentration. The extract prevented lipid peroxidation in a dose-dependent 5. The effect of Mori Folium extract on reactive oxygen species(ROS) generation was examined using a celt-free system induced by hydrogen peroxide FeSO$_4$. Addition of 1 mg/ml of Mori Folium extract significantly reduced dichlorofluorescein(DCf) fluorescence. The extract caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that the extract significantly prevented ROS generation in vitro. Conclusion ; The antioxidant effects of Mori Folium extract seem to be due, at least in part, to the prevention offree radical-induced oxidation, fllowed by inhibition of lipid peroxidation.

• Clinical Nutrition Research
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• v.12 no.4
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• pp.257-268
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• 2023

Migraine is a common neurological disease correlated with oxidative stress and lipid profile disorders. The present study was designed to determine the effects of Coenzyme Q10 (Co-Q10) supplementation on oxidative status and lipid profile in migraine individuals. This clinical trial was conducted on 84 females aged 18-50 years, diagnosed for episodic migraine according to the International Headache Society. Subjects were randomized to receive either Co-Q10 supplement (400 mg/day) or placebo for 12 weeks. Lipid profile and oxidative stress indices including malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured before and after intervention in both groups. Also, anthropometric indices, dietary intakes, and clinical features were collected. Data analysis was conducted using SPSS version 16. Seventy-seven of the participants, with mean age of 33.70 ± 7.75 years, completed the study. After 12-week intervention, Co-Q10 led to a significant decrease in MDA levels compared to placebo (p = 0.009), with no effect on TAC levels (p = 0.106). A significant increase in serum Co-Q10 concentration and high-density lipoprotein cholesterol (HDL-C) level in Co-Q10 group was observed, but no significant differences were found in other lipid profile variables (low-density lipoprotein cholesterol, triglycerides and total cholesterol). Among anthropometric variables, Co-Q10 only caused a significant reduction in body fat percentage (BFP), but we did not find any significant changes in others. A 12-week Co-Q10 supplementation led to significant improvement in clinical features, BFP, and HDL-C level among migraine individuals.

• Fisheries and Aquatic Sciences
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• v.4 no.2
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• pp.88-92
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• 2001

To examine effects of cadmium on the respiratory burst of kidney phagocytes and antioxidant defense in liver, juvenile red seabream Pagrus major were fed a cadmium-incorporated diet $(1g\;CdC1_2/kg\;diet)$. The respiratory burst activity measured by chemiluminescence (CL) was significantly reduced by oral intake of cadmium. Lipid peroxidation in liver expressed as thiobarbituric acid reactive substances (TBARS) was significantly higher in the fish fed a cadmium-incorporated diet than that of the fish fed a control diet both on Day 3 and Day 9. Liver Glutathione S-transferase (GST) activitiy was significantly increased both on Day 3 and Day 9 by feeding a cadmium-incorporated diet, when compared with the controls. From the present results, it can be concluded that oral intake of cadmium in red seabream is associated with marked reduction of respiratory burst capacity of kidney phagocytes which can elevate susceptibility of fish against infecting pathogens. Cadmium administration also elicits significant increment of lipid peroxidation in liver, and fish try to detoxify cadmium by increasing GST activity.

• Journal of Nutrition and Health
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• v.31 no.4
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• pp.687-696
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• 1998

This study was performed to investigate effects of hesperidin and naringin on linpid peroxide formation and antioxidative enzyme activities in rats. Thiobarbituric acid reactive substance (TBARS) concentrations were measured in plasma and liver. Catalase, superoxide dismutase, and glutathione peroxidase activities were measured in erythrocyte and liver. Forty-nine male Sprague-Dauley rats weighing 275.3$\pm$3.3g were blocked into seven groups according to body weight and were raised fro four weeks on diets containing 0.25, 0.50 or 1.00%(w/w) hesperidin or naringin . Food intake, weight gain , food efficiency ratio, and weights of liver, kidney, spleen ,and epididymal fat pad were not significantly different among groups. In 0.50 and 1.00% naringin groups , plasma TBARS concentrations were significantly decreased with a dose response patter. In 0.25, 0.50 and 1.00% hesperidin groups, liver TBARS concentrations were significantly decreased without a dose dependent patter. Antiosidative enzyme activities in erythrocyte and liver were not significantly affected by type and amountof dietary bioflavonoid, but in the 1.00% hesperidin group, catalase, superoxide dismutase, and glutahione perosidase activities in linver showed a tendency to increase. In conclusion, naringin inhibited lipid peroxide formation with a dose response pattern in plasma without changing the activities of antioxidative enzymes. Hesperidin adminstration, regardless of the level in the diet, inhibited lipid peroxide formation in liver.