Antioxidant effects of a dietary supplement: Reduction of indices of oxidative stress in normal subjects by water-soluble chitosan

2009 ◽  
Vol 47 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Makoto Anraku ◽  
Takeshi Fujii ◽  
Nobuko Furutani ◽  
Daisuke Kadowaki ◽  
Toru Maruyama ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dietary Supplement ◽  
Normal Subjects ◽  
Water Soluble ◽  
Antioxidant Effects

scholarly journals Novel Insights into the Regulatory Role of Nuclear Factor (Erythroid-Derived 2)-Like 2 in Oxidative Stress and Inflammation of Human Fetal Membranes

2020 ◽  
Vol 21 (17) ◽  
pp. 6139 ◽  
Author(s):  
Ramkumar Menon ◽  
Morgan R Peltier
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Water Soluble ◽  
Fetal Membrane ◽  
Fetal Membranes ◽  
Peroxisome Proliferator ◽  
Nuclear Factor ◽  
Western Blots ◽  
Adverse Pregnancy ◽  
Nrf2 Expression

Fetal membrane dysfunction in response to oxidative stress (OS) is associated with adverse pregnancy outcomes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is one of the regulators of innate OS response. This study evaluated changes in Nrf2 expression and its downstream targets heme oxygenase (HO-1) and peroxisome proliferator-activated receptor gamma (PPARγ) in fetal membranes during OS and infection in vitro. Furthermore, we tested the roles of sulforaphane (SFN; an extract from cruciferous vegetables) and trigonelline (TRN; an aromatic compound in coffee) in regulating Nrf2 and its targets. Fetal membranes (n = 6) collected at term were placed in an organ explant system were treated with water-soluble cigarette smoke extract (CSE), an OS inducer (1:10), and lipopolysaccharide (LPS; 100 ng/mL). Nrf2 expression, expression, its enhancement by sulforaphane (SFN, 10 µM/mL) and down regulation by TRN (10uM/mL) was determined by western blots. Expression of Nrf2 response elements PPARγ (western) heme oxygenase (HO-1), and IL-6 were quantified by ELISA. CSE and LPS treatment of fetal membranes increased nrf2, but reduced HO-1 and PPARγ and increased IL-6. Co-treatment of SFN, but not with TRN, with CSE and LPS increased Nrf2 substantially, as well as increased HO-1 and PPARγ and reduced IL-6 expression. Risk factor-induced Nrf2 increase is insufficient to generate an antioxidant response in fetal membranes. Sulforaphane may enhance innate antioxidant and anti-inflammatory capacity by increasing NRF-2 expression.

scholarly journals Phytochemical Analysis of Anti-Inflammatory and Antioxidant Effects of Mahonia aquifolium Flower and Fruit Extracts

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Andra-Diana Andreicut ◽  
Alina Elena Pârvu ◽  
Augustin Cătălin Mot ◽  
Marcel Pârvu ◽  
Eva Fischer Fodor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Stress Index ◽  
Tnf Alpha ◽  
Phytochemical Analysis ◽  
Anti Inflammatory ◽  
Mahonia Aquifolium ◽  
Antioxidant Effects

Oxidative stress and inflammation are interlinked processes. The aim of the study was to perform a phytochemical analysis and to evaluate the antioxidant and anti-inflammatory activities of ethanolic Mahonia aquifolium flower (MF), green fruit (MGF), and ripe fruit (MRF) extracts. Plant extract chemical composition was evaluated by HLPC. A DPPH test was used for the in vitro antioxidant activity. The in vivo antioxidant effects and the anti-inflammatory potential were tested on a rat turpentine oil-induced inflammation, by measuring serum nitric oxide (NOx) and TNF-alpha, total oxidative status (TOS), total antioxidant reactivity (TAR), oxidative stress index (OSI), 3-nitrothyrosine (3NT), malondialdehyde (MDA), and total thiols (SH). Extracts were administrated orally in three dilutions (100%, 50%, and 25%) for seven days prior to inflammation. The effects were compared to diclofenac. The HPLC polyphenol and alkaloid analysis revealed chlorogenic acid as the most abundant compound. All extracts had a good in vitro antioxidant activity, decreased NOx, TOS, and 3NT, and increased SH. TNF-alpha was reduced, and TAR increased only by MF and MGF. MDA was not influenced. Our findings suggest that M. aquifolium has anti-inflammatory and antioxidant effects that support the use in primary prevention of the inflammatory processes.

Insights into the Relation between Oxidative Stress and Malaria: A Mechanistic and Therapeutic Approach

2021 ◽  
Vol 11 ◽  
Author(s):  
Abhijit Sarkar ◽  
Swarnendu Basak ◽  
Sumit Ghosh ◽  
Sushweta Mahalanobish ◽  
Parames C. Sil
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Preventive Measures ◽  
Host Immunity ◽  
Malarial Parasite ◽  
Malarial Infection ◽  
Parasitic Load ◽  
Therapeutic Mechanisms ◽  
Antioxidant Effects ◽  
Oxidative Insult

The mortality rate due to malaria has increased tremendously in the last decade. Even though the causative agent of this disease is known, the preventive measures are not potent enough to control the spread of this disease. Malarial infection involves a strong interrelationship between oxidative stress and pathogenesis. This review addresses the various oxidative stress-related mechanisms associated with vector defense, host immunity, plasmodial pathogenesis, and corresponding therapeutic strategies. The mechanisms involving host and vector defense show both similarity and contradiction to the processes involving plasmodial pathogenesis under different circumstances. Therefore, corresponding ameliorative peculiarities are observed in the therapeutic mechanisms adopted by the anti-malarial drugs. The malarial parasite augments oxidative stress to weaken the host and exerts antioxidant effects against host defense mechanisms. However, the anti-malarial drugs induce oxidative insult to reduce parasitic load and exert antioxidant effects against parasite infection-induced oxidative stress in host. Thus, the anti-malarial drugs exhibit antioxidant activity in hosts and/or pro-oxidant activity in parasites.

scholarly journals A Water-Soluble Fullerene Vesicle Alleviates Angiotensin II-Induced Oxidative Stress in Human Umbilical Venous Endothelial Cells

2008 ◽  
Vol 31 (1) ◽  
pp. 141-151 ◽  
Author(s):  
Rui MAEDA ◽  
Eisei NOIRI ◽  
Hiroyuki ISOBE ◽  
Tatsuya HOMMA ◽  
Tamami TANAKA ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Water Soluble

scholarly journals Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0233425 ◽  
Author(s):  
Zaira Leni ◽  
Laure Estelle Cassagnes ◽  
Kaspar R. Daellenbach ◽  
Imad El Haddad ◽  
Athanasia Vlachou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Mediators ◽  
Apical Cell ◽  
Ambient Air ◽  
Water Soluble ◽  
Ambient Air Pollution ◽  
Anthropogenic Aerosol ◽  
Bronchial Epithelia ◽  
Clear Dose Response ◽  
The Impact

Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9–2.5 and 8.8–25.4 μg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population.

The effects of a water-soluble alpha tetra-substituted zinc phthalocyanine derivative onArthrospira platensis-M2 strain

2018 ◽  
Vol 22 (08) ◽  
pp. 686-692 ◽  
Author(s):  
Armağan Günsel ◽  
Hatice Tunca ◽  
Ahmet T. Bilgiçli ◽  
Ali Doğru ◽  
M. Nilüfer Yaraşir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Biomass Accumulation ◽  
Arthrospira Platensis ◽  
Water Soluble ◽  
Zinc Phthalocyanine ◽  
Natural Environments ◽  
Oxygen Species ◽  
Sod Activity ◽  
Future Studies

In this study, we have analyzed the effect a newly synthesized water-soluble alpha tetra-substituted zinc phthalocyanine (Pc) compound on superoxide dismutase (SOD), ascorbate peroxidase (APX) and glutathione reductase (GR) activities and biomass accumulation in the Arthrospira platensis-M2 strain to test whether this compound could be used as an algaecide or not. We found that lower concentrations (3 μg mL[Formula: see text] and 6 μg mL[Formula: see text] of Pc compound were not toxic to algae cells, as indicated by enduring biomass accumulation during the study (7 days). Higher Pc concentrations, however, were toxic and inhibited biomass accumulation. This inhibition appeared on the fourth day and persisted during the study. At higher Pc concentrations, SOD activity decreased significantly, but APX and GR activity were not affected. These results may show that Pc applications did not cause the accumulation of reactive oxygen species in Arthrospira platensis-M2 cells. Our result suggests that higher Pc concentrations did not cause oxidative stress but biomass accumulation inhibited, possibly due to some different toxicity mechanism(s), which should be carried out in the future studies. As a result, we may offer use of this compound as a means to keep under control algal populations in natural environments.

scholarly journals Withaferin A Exerts Preventive Effect on Liver Fibrosis through Oxidative Stress Inhibition in a Sirtuin 3-Dependent Manner

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Jingya Gu ◽  
Chang Chen ◽  
Jue Wang ◽  
Tingting Chen ◽  
Wenjuan Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Withaferin A ◽  
Dependent Manner ◽  
Sirtuin 3 ◽  
Antifibrogenic Effect ◽  
Antioxidant Effects ◽  
Sirt3 Expression ◽  
Bioactive Constituent

Sirtuin 3 (SIRT3) is a deacetylase involved in the development of many inflammation-related diseases including liver fibrosis. Withaferin A (WFA) is a bioactive constituent derived from the Withania somnifera plant, which has extensive pharmacological activities; however, little is known about the regulatory role of SIRT3 in the WFA-induced antifibrogenic effect. The current study is aimed at investigating the role of SIRT3 in WFA-induced antioxidant effects in liver fibrosis. Our study verified that WFA attenuated platelet-derived growth factor BB- (PDGF-BB-) induced liver fibrosis and promoted PDGF-BB-induced SIRT3 activity and expression in JS1 cells. SIRT3 silencing attenuated the antifibrogenic and antioxidant effects of WFA in activated JS1 cells. Moreover, WFA inhibited carbon tetrachloride- (CCl4-) induced liver injury, collagen deposition, and fibrosis; increased the SIRT3 expression; and suppressed the CCl4-induced oxidative stress in fibrotic livers of C57/BL6 mice. Furthermore, the antifibrogenic and antioxidant effects of WFA could be available in CCl4-induced WT (129S1/SvImJ) mice but were unavailable in CCl4-induced SIRT3 knockout (KO) mice. Our study suggested that WFA inhibited liver fibrosis through the inhibition of oxidative stress in a SIRT3-dependent manner. WFA could be a potential compound for the treatment of liver fibrosis.

Oxidative stress induced by urban fine particles in cultured EA.hy926 cells

2010 ◽  
Vol 30 (7) ◽  
pp. 579-590 ◽  
Author(s):  
Han Wei ◽  
Dan Wei ◽  
Shuo Yi ◽  
Fang Zhang ◽  
Wenjun Ding
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Fine Particles ◽  
Cell Damage ◽  
Umbilical Vein ◽  
Direct Interaction ◽  
Water Soluble ◽  
Apoptotic Pathway ◽  
Metal Elements ◽  
Ea.Hy926 Cells

It has been reported that vascular endothelia cell damage is an important precursor to the morbidity and mortality associated with cardiovascular disease exposed to airborne particulate matter (PM). The present study investigated the hypothesis that urban fine (PM2.5) particles could cause cytotoxicity via oxidative stress in human umbilical vein endothelial cells, EA.hy926. The concentrations of metal elements (Cr, Fe, Ni, Cu, Zn, Mo, Cd and Pb) in PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 were determined by inductively coupled plasma - mass spectrometry (ICP-MS). Iron (Fe), Zn and Pb were highly enriched in all the samples. Exposure of the cultured EA.hy926 cells to PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 led to cell death, reactive oxygen species (ROS) increase, mitochondrial transmembrane potential (ΔΨm) disruption and NF-κB activation, respectively. The ROS increase by exposure to PM 2.5 suspension, water-soluble and water-insoluble fractions of PM 2.5 triggered the activation of nuclear factor (NF)-κB, which means that PM2.5 particles exert cytotoxicity by an apopotic process. However, the induction of cytotoxicity by PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 was reversed by pretreatment with superoxide dismutase (SOD). These results suggest that each fraction of PM2.5 has a potency to cause oxidative stress in endothelial cells. ROS was generated through PM2.5-mediated mitochondrial apoptotic pathway, which may induce direct interaction between metal elements and endothelia cells.

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