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Doxorubicin (DOX) induces oxidative stress leading to cardiotoxicity. Diosgenin, a steroidal saponin of Dioscorea opposita, has been reported to have antioxidant activity. Our study was aimed to find out the protective effect of diosgenin against DOX-induced cardiotoxicity in mice. DOX treatment led to a significant decrease in the ratio of heart weight to body weight, and increases in the blood pressure and the serum levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and creatine kinase myocardial bound (CK-MB), markers of cardiotoxicity. In the heart tissue of the DOX-treated mice, DOX reduced activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), were recovered by diosgenin. Diosgenin also decreased the serum levels of cardiotoxicity markers, cardiac levels of thiobarbituric acid relative substances (TBARS) and reactive oxygen species (ROS), caspase-3 activation, and mitochondrial dysfunction, as well as the expression of nuclear factor kappa B (NF-κB), an inflammatory factor. Moreover, diosgenin had the effects of increasing the cardiac levels of cGMP via modulation of phosphodiesterase-5 (PDE5) activity, and in improving myocardial fibrosis in the DOX-treated mice. Molecular data showed that the protective effects of diosgenin might be mediated via regulation of protein kinase A (PKA) and p38. Our data imply that diosgenin possesses antioxidant and anti-apoptotic activities, and cGMP modulation effect, which in turn protect the heart from the DOX-induced cardiotoxicity.

Background & Aims: The impact of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection upon B vitamins status and antioxidative defense in infected patients was examined., Methods: Dietary record and blood levels of B vitamins and oxidative stress-associated biomarkers were determined for 195 healthy controls, 132 HBV, and 114 HCV patients., Results: HBV-infected patients had significantly higher levels of total cholesterol, free fatty acids (FFA), and lower ghrelin level (p < 0.05); and HCV-infected patients had significantly higher Ishak inflammation score and lactate dehydrogenase activity (p < 0.05). HBV patients had significantly lower red blood cell (RBC) vitamins B(2) and B(6) levels, and HCV infection significantly decreased vitamins B(2,) B(6) and folate levels in RBC and/or plasma (p < 0.05). Correlation coefficients of RBC vitamin B(2) versus serum FFA in HBV patients, RBC vitamins B(2) and B(6) versus HCV RNA and Ishak inflammation score, and plasma vitamin B(6) vs Ishak inflammation score in HCV patients were <-0.5. HBV-infected patients had significantly higher oxidized glutathione level and lower glutathione peroxidase activity (p < 0.05), but HCV patients had significantly lower superoxide dismutase and catalase activities (p < 0.05)., Conclusion: HBV or HCV infection enhanced oxidative stress and lowered B vitamins in circulation. In order to avoid other healthy risk, nutrition status should be monitored and limitation or supplementation of certain nutrients might be helpful for HBV- or HCV-infected patients.

Background: This study analysed the content of ascorbic acid, phenolic acids and flavonoids in aqueous and ethanol extracts of pepino (Solanum muricatum Ait.), and examined the protective effects of pepino aqueous extract (PAE) in a mouse model of diabetes. PAE at 1, 2 and 4% was supplied for 5 weeks., Results: Aqueous and ethanol extracts had similar levels of total phenolic acids, but PAE had a higher content of ascorbic acid and total flavonoids than the ethanol extract. PAE treatments at 2% and 4% significantly lowered plasma glucose level (P < 0.05); however, only the 4% PAE significantly elevated plasma insulin level at week 5 (P < 0.05). PAE treatments significantly decreased the levels of malonyldialdehyde and reactive oxygen species in kidney (P < 0.05); however, only the 2% and 4% treatments significantly reduced oxidised glutathione formation, increased glutathione level, and retained renal glutathione peroxidase and catalase activities (P < 0.05). PAE treatments at 2% and 4% significantly lowered renal interleukin (IL)-6 and tumour necrosis factor-α levels (P < 0.05); however, only the 4% treatments significantly diminished renal IL-1β and levels of monocyte chemoattractant protein-1 (P < 0.05). PAE treatments at 4% significantly decreased aldose reductase activity and sorbitol production in kidney (P < 0.05)., Conclusion: These findings support the suggestion that pepino aqueous extract could attenuate the progression of diabetes via its antioxidative, anti-inflammatory and antiglycative effects., (Copyright © 2011 Society of Chemical Industry.)

We elucidated the cytoprotective effects of hyperoside (quercetin-3-O-galactoside) against hydrogen peroxide (H2O2)-induced cell damage. We found that hyperoside scavenged the intracellular reactive oxygen species (ROS) detected by fluorescence spectrometry, flow cytometry, and confocal microscopy. In addition, we found that hyperoside scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO4)+H2O2) in a cell-free system, which was detected by electron spin resonance (ESR) spectrometry. Hyperoside was found to inhibit H2O2-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic nuclear fragmentation, decreased sub-G(1) cell population, and decreased DNA fragmentation. In addition, hyperoside pretreatment inhibited the H2O2-induced activation of caspase-3 measured in terms of levels of cleaved caspase-3. Hyperoside prevented H2O2-induced lipid peroxidation as well as protein carbonyl. In addition, hyperoside prevented the H2O2-induced cellular DNA damage, which was established by comet tail, and phospho histone H2A.X expression. Furthermore, hyperoside increased the catalase and glutathione peroxidase activities. Conversely, the catalase inhibitor abolished the cytoprotective effect of hyperoside from H2O2-induced cell damage. In conclusion, hyperoside was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing antioxidant enzyme activity.

Aim: To investigate the anti-oxidant properties of esculetin (6,7-dihydroxycoumarin) against H2O2-induced Chinese hamster lung fibroblast (V79-4) damage., Methods: The radical scavenging activity was assessed by 1,1-diphenyl- 2-picrylhydrazyl (DPPH) radical, hydroxyl radical, and intracellular reactive oxygen species (ROS). In addition, lipid peroxidation was assayed by the measure of related substances which react with thiobarbituric acid. The amount of carbonyl formation in protein was determined using a protein carbonyl ELISA kit. As well, cellular DNA damage was detected by Western blot and immunofluorescence image. Cell viability was assessed by 3-(4,5-dimethylthiazole-2- yl)-2,5-diphenyltetrazolium bromide assay., Results: Esculetin exhibited DPPH radical scavenging, hydroxyl radical scavenging, and intracellular ROS scavenging activities. The radical scavenging activity of esculetin resulted in the protection of cells from lipid peroxidation, protein carbonyl, and DNA damage induced by H2O2. Therefore, esculetin recovered cell viability exposed to H2O2., Conclusion: Esculetin efficiently attenuated the oxidative stress induced cell damage via its anti-oxidant properties. As a result, esculetin may be useful in the development of functional food and raw materials of medicine.

The antioxidant property of butin was investigated for cytoprotective effect against H(2)O(2)-induced cell damage. This compound showed intracellular reactive oxygen species (ROS) scavenging, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging, inhibition of lipid peroxidation, and DNA damage. This radical scavenging activity of butin protected cell damage exposed to H(2)O(2). Also, butin reduced the apoptotic cells induced by H(2)O(2), as demonstrated by the decreased DNA fragmentation, apoptotic body formation, and caspase 3 activity. In addition, butin restored the activity and protein expression of cellular antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) in H(2)O(2)-treated cells. Taken together, these findings suggest that butin protected cells against H(2)O(2)-induced cell damage via antioxidant property.

The protective properties of irisolidone (a metabolite of kakkalide by intestinal bacteria) against hydrogen peroxide (H(2)O(2)) induced cell damage were investigated. Irisolidone was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and the intracellular reactive oxygen species (ROS), thereby preventing lipid peroxidation and DNA damage. Irisolidone inhibited apoptosis in Chinese hamster lung fibroblast (V79-4) cells induced by H(2)O(2) via radical scavenging activity. This was achieved by the activation of the extracellular signal regulated kinase (ERK) and DNA binding activity of activator protein-1 (AP-1) (a downstream transcription factor of ERK) by irisolidone.

Objective: To examine the differences in food and antioxidant vitamin intake in current non-smokers,light smokers,and heavy smokers., Methods: 51 115 people (24 077 male, 27 038 female) aged above 15 years who had completed providing information on smoking habit and dietary intake, were selected from 2002 national health and nutrition survey., Results: After adjustment for geographic areas and age, data showed the smokers ate more light vegetable and alcohol, less dark vegetable and fruit than non-smokers. Male smokers consumed more energetic stuff and macronutrients than non-smokers, but female smokers had opposite trends. Light smokers (LS) consumed less antioxidant than non-smokers (NS) after adjusted for area, age, BMI and energy, with carotene (Male LS = 1824.7 microg, NS = 1964.8 microg; Female LS = 1565.4 microg, NS = 2127.4 microg), thiamin (Male LS = 0.84 mg, NS = 0.85 mg; Female LS = 0.72 mg, NS = 0.74 mg), vitamin E (alpha) (Male LS = 9.2 mg, NS = 9.3 mg; Female LS = 7.4 mg, NS = 8.1 mg), vitamin C (Male LS = 91.2 mg, NS = 94.2 mg; Female LS = 76.9 mg, NS = 87.5 mg)., Conclusion: Smokers had a significantly lower overall mean dietary antioxidant vitamin intake than non-smokers. Increasing the daily consumption of variety of fruits and vegetables had been recommended to reduce the risk of chronic diseases.

Abstract: We evaluated the cytoprotective effect of myricetin on oxidative stress damaged cells by assessment of the scavenging effect of reactive oxygen species (ROS) and the activities of antioxidant enzymes. Myricetin showed the scavenging effect of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals on intracellular ROS. In addition, myricetin restored the activity and protein expression of cellular antioxidant defense enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) reduced by hydrogen peroxide (H2O2) treatment. H2O2-induced cellular DNA and lipid damages, and myricetin was found to prevent the DNA damage shown by inhibition of DNA tail and it decreased nuclear phospho-histone H2A.X expression, which are both markers for DNA strand breakage. Membrane lipid peroxidation was also attenuated as shown by inhibition of TBARS formation and of fluorescence intensity of diphenyl-1-pyrenylphosphine (DPPP). These results suggest that myricetin protects cells against H2O2-induced cell damage via inhibition of ROS generation and activation of antioxidant enzymes. [Copyright &y& Elsevier]

Chronic itch is a distressing symptom of many skin diseases and negatively impacts quality of life. However, there is no medication for most forms of chronic itch, although antihistamines are often used for anti-itch treatment. Epigallocatechin-3-gallate (EGCG), a major green tea polyphenol, exhibits anti-oxidative and anti-inflammatory properties. Our previous studies highlighted a key role of oxidative stress and proinflammatory cytokines in acute and chronic itch. Here, we evaluated the effects of green tea polyphenon 60 and EGCG on acute and chronic itch in mouse models and explored its potential mechanisms. The effects of EGCG were determined by behavioral tests in mouse models of acute and chronic itch, which were induced by compound 48/80, chloroquine (CQ), and 5% imiquimod cream treatment, respectively. We found that systemic or local administration of green tea polyphenon 60 or EGCG significantly alleviated compound 48/80- and chloroquine-induced acute itch in a dose-dependent manner in mice. Incubation of EGCG significantly decreased the accumulation of intracellular reactive oxygen species (ROS) directly induced by compound 48/80 and CQ in cultured ND7-23 cells, a dorsal root ganglia derived cell line. EGCG also attenuated imiquimod-induced chronic psoriatic itch behaviors and skin epidermal hyperplasia in mice. In addition, EGCG inhibited the expression of IL-23 mRNA in skin and TRPV1 mRNA in dorsal root ganglia (DRG). Finally, EGCG remarkably inhibited compound 48/80-induced phosphorylation of extracellular signal-regulated kinase (ERK) and imiquimod-induced p-AKT in the spinal cord of mice, respectively. Collectively, these results indicated EGCG could be a promising strategy for anti-itch therapy. [ABSTRACT FROM AUTHOR]

Abstract: The antioxidant potential of 1,2,3,4,6-penta-O-galloyl-β-d-glucose (PGG), isolated from Elaeocarpus sylvestris var. ellipticus, was investigated by various established systems based on cell-free and cell system experiments, such as radical detection, antioxidant enzyme assay, lipid peroxidation detection, and cell viability assay. PGG was found to quench the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and intracellular reactive oxygen species. PGG recovered the cellular antioxidant enzyme activities of superoxide dismutase, catalase, and glutathione peroxidase, which were reduced by H2O2 treatment, thereby resulting in the inhibition of lipid peroxidation. Cytoprotective effects of PGG were based on the results of DNA fragmentation, mitochondrial membrane potential (Δψ), apoptotic body formation, and caspase-3 activity. The results suggest that PGG protects cells against H2O2-induced cell damage via antioxidant properties. [Copyright &y& Elsevier]