scholarly journals Supernatants of Bifidobacterium longum and Lactobacillus plantarum Strains Exhibited Antioxidative Effects on A7R5 Cells

2021 ◽  
Vol 9 (2) ◽  
pp. 452
Author(s):  
Yusheng Wang ◽  
Zhifeng Fang ◽  
Qixiao Zhai ◽  
Shumao Cui ◽  
Jianxin Zhao ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Protein Biosynthesis ◽  
Bifidobacterium Longum ◽  
Sod Activity ◽  
Expression Of Genes ◽  
A7r5 Cells ◽  
Antioxidative Effects ◽  
Probiotic Strains ◽  
Nadph Oxidase Activation

Vascular reactive oxygen species (ROS) play an essential role in cardiovascular diseases and the antioxidative effects of probiotics have been widely reported. To screen the probiotic strains that may prevent cardiovascular diseases, we tested the antioxidative effects of supernatants of different Bifidobacterium and Lactobacillus strains on A7R5 cells. Preincubation with supernatants of B. longum CCFM752, L. plantarum CCFM1149, or L. plantarum CCFM10 significantly suppressed the angiotensin II-induced increases in ROS levels and increased catalase (CAT) activity in A7R5, whereas CCFM752 inhibited NADPH oxidase activation and CCFM1149 enhanced the intracellular superoxide dismutase (SOD) activity simultaneously. Treatment with CCFM752, CCFM1149, or CCFM10 supernatants had no significant impact on transcriptional levels of Cat, Sod1, Sod2, Nox1, p22phox, or p47phox, but altered the overall transcriptomic profile and the expression of genes relevant to protein biosynthesis, and up-regulated the 60S ribosomal protein L7a (Rpl7a). A positive correlation between Rpl7a expression and intracellular CAT activity implied that Rpl7a may participate in CAT synthesis in A7R5. Supernatant of CCFM752 could also down-regulate the expression of NADPH oxidase activator 1 (Noxa1) and angiotensinogen in A7R5. Collectively, the probiotic strains CCFM752, CCFM1149, and CCFM10 exhibited antioxidative attributes on A7R5 cells and might help to reduce the risk of cardiovascular diseases.

scholarly journals Attenuation of renal excretory responses to ANG II during inhibition of superoxide dismutase in anesthetized rats

2010 ◽  
Vol 298 (2) ◽  
pp. F401-F407 ◽  
Author(s):  
Md. Abdul Hye Khan ◽  
Mohammed Toriqul Islam ◽  
Alexander Castillo ◽  
Dewan Syed Abdul Majid
Keyword(s):  
Superoxide Dismutase ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Ang Ii ◽  
Sod Activity ◽  
Doppler Flowmetry ◽  
Nadph Oxidase Activity ◽  
Blood Flows ◽  
Renal Responses

To examine the functional interaction between superoxide dismutase (SOD) and NADPH oxidase activity, we assessed renal responses to acute intra-arterial infusion of ANG II (0.5 ng·kg−1·min−1) before and during administration of a SOD inhibitor, diethyldithiocarbamate (DETC, 0.5 mg·kg−1·min−1), in enalaprilat-pretreated (33 μg·kg−1·min−1) rats ( n = 11). Total (RBF) and regional (cortical, CBF; medullary; MBF) renal blood flows were determined by Transonic and laser-Doppler flowmetry, respectively. Renal cortical and medullary tissue NADPH oxidase activity in vitro was determined using the lucigenin-chemiluminescence method. DETC treatment alone resulted in decreases in RBF, CBF, MBF, glomerular filtration rate (GFR), urine flow (V), and sodium excretion (UNaV) as reported previously. Before DETC, ANG II infusion decreased RBF (−18 ± 3%), CBF (−16 ± 3%), MBF [−5 ± 6%; P = not significant (NS)], GFR (−31 ± 4%), V (−34 ± 2%), and UNaV (−53 ± 3%). During DETC infusion, ANG II also caused similar reductions in RBF (−20 ± 4%), CBF (−19 ± 3%), MBF (−2 ± 2; P = NS), and in GFR (−22 ± 7%), whereas renal excretory responses (V; −12 ± 2%; UNaV; −24 ± 4%) were significantly attenuated compared with those before DETC. In in vitro experiments, ANG II (100 μM) enhanced NADPH oxidase activity both in cortical [13,194 ± 1,651 vs. 20,914 ± 2,769 relative light units (RLU)/mg protein] and in medullary (21,296 ± 2,244 vs. 30,597 ± 4,250 RLU/mg protein) tissue. Application of DETC (1 mM) reduced the basal levels and prevented ANG II-induced increases in NADPH oxidase activity in both tissues. These results demonstrate that renal excretory responses to acute ANG II administration are attenuated during SOD inhibition, which seems related to a downregulation of NADPH oxidase in the deficient condition of SOD activity.

Protein kinase C-α and -δ are required for NADPH oxidase activation in WKYMVm-stimulated IMR90 human fibroblasts

2007 ◽  
Vol 459 (2) ◽  
pp. 288-294 ◽  
Author(s):  
Annalisa Iaccio ◽  
Claudio Collinet ◽  
Nicola Montesano Gesualdi ◽  
Rosario Ammendola
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Nadph Oxidase ◽  
Human Fibroblasts ◽  
Kinase C ◽  
Nadph Oxidase Activation

Abstract 107: Apocynin Attenuates Isoproterenol-induced Myocardial Injury: Implications For Targeting Nadph Oxidase In Myocardial Fibrogenesis

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Yu Chen ◽  
Jingang Cui ◽  
Qinbo Yang ◽  
Chenglin Jia ◽  
Minqi Xiong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Myocardial Fibrosis ◽  
Myocardial Injury ◽  
Oxidase Inhibitor ◽  
Ros Generation ◽  
Dependent Manner ◽  
Expression Of Genes ◽  
Therapeutic Development ◽  
Myocardial Injuries

Myocardial fibrosis results from cardiac injuries caused by various pathophysiological mechanisms including myocardial infarction, leading to destruction of myocardial architecture and progressive cardiac dysfunction. Oxidative stress is likely involved in myocardial ischemic injury and the subsequent tissue remodeling mediated by myocardial fibrogenesis. Our current study aimed to evaluate the implication of NADPH oxidase in overproduction of reactive oxygen species and its contribution to the pathogenesis of myocardial fibrogenesis after ischemic injuries. The effects of Apocynin, a selective NADPH oxidase inhibitor, were evaluated in the mouse model of isoproterenol-induced myocardial injury by histopathological approaches and whole-genome gene expression profiling. The results demonstrated that Apocynin was able to inhibit the development of ISO-induced myocardial necrotic lesions and fibrogenesis in a dose-dependent manner. Moreover, the preventive effects of Apocynin on myocardial injuries were associated with suppressed expression of genes implicated in inflammation responses and extracellular matrix, which were remarkably upregulated by isoproterenol administration. In summary, o ur study provides proof-of-concept for the involvement of NADPH oxidase-mediated ROS generation in myocardial ischemic injuries and fibrogenesis, which will benefit the mechanism-based therapeutic development targeting NADPH oxidase and oxidative stress in treating myocardial fibrosis and related disorders.

The effect of cadaverine on redox homeostasis of wheat seedling roots and their resistance to damage heating

2021 ◽  
pp. 116-137
Author(s):  
Alexandr I. Kokorev ◽  
◽  
Yuriy E. Kolupaev ◽  
Maxim A. Shkliarevskyi ◽  
Anna A. Lugovaya ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Antioxidant Enzymes ◽  
Nadph Oxidase ◽  
Diamine Oxidase ◽  
Oxidase Inhibitor ◽  
Guaiacol Peroxidase ◽  
Sod Activity ◽  
Wheat Seedlings ◽  
Nadph Oxidase Inhibitor ◽  
Survival Of Seedlings

Polyamines are plant metabolites involved in many processes under physiologically normal and stressful conditions. Cadaverine is one of the least studied plant polyamines. The relationship between its physiological effects and the formation of signaling mediators, in particular, reactive oxygen species (ROS), has hardly been specially studied. The aim of this work was to study the possible protective effect of cadaverine on wheat (Triticum aestivum L.) seedlings under heat stress and its relationship with the formation and detoxification of ROS by antioxidant enzymes. Etiolated seedlings of soft winter wheat variety Doskonala were used in the work. We treated three-day-old seedlings with cadaverine at concentrations ranging from 0.05 to 2.5 mM by adding it to the root incubation medium. In some variants of the experiment, we treated seedlings with a hydrogen peroxide scavenger dimethylthiourea (DMTU - 150 μM), a diamine oxidase inhibitor aminogunidine (1 mM) or an inhibitor NADPH oxidase imidazole (10 μM), as well as the indicated inhibitors in combination with cadaverine. The hydrogen peroxide content and the activity of antioxidant enzymes were determined in the roots of seedlings a certain time after treatment with the studied compounds. One day after the treatment of seedlings with cadaverine, ROS antagonists, and a combination of effectors, the seedlings were subjected to damaging heating in a water thermostat (10 min at 45 °C). 24 h after heating, we assessed the content of the products of lipid peroxidation (LPO) in the roots and, after 3 days, the survival of seedlings. Incubation in the presence of cadaverine increased the resistance of seedlings to damaging heat (See Fig. 1). The highest relative number of surviving seedlings was observed in the variant with 1 mM cadaverine treatment. Under the effect of cadaverine, the content of hydrogen peroxide in the roots increased (See Fig. 2). We observed a noticeable effect 1-4 h after the start of treatment, with a maximum after 2 h. Treatment of seedlings with a scavenger of hydrogen peroxide DMTU removed the manifestation of the effect of an increase in the content of H2 O2 in the roots caused by the action of cadaverine (See Fig. 3). This effect was also completely eliminated by the diamine oxidase inhibitor aminoguanidine and was almost unchanged in the presence of the NADPH oxidase inhibitor imidazole. The effect of heat stress on seedlings caused an increase in the content of the LPO products in them. Treatment with cadaverine markedly reduced this manifestation of oxidative stress. The antioxidant DMTU and the diamine oxidase inhibitor aminoguanidine largely neutralized the protective effect of cadaverine (See Fig. 4a). At the same time, the NADPH oxidase inhibitor imidazole had almost no effect on the manifestation of the effect of cadaverine on the LPO products content in roots. Under the influence of DMTU and aminoguanidine, but not imidazole, the positive effect of cadaverine on the survival of seedlings after damaging heating was also leveled out (See Fig. 4b). The treatment of seedlings with cadaverine caused a change in the activity of antioxidant enzymes in the roots (superoxide dismutase - SOD, catalase, and guaiacol peroxidase) (See Fig. 5). DMTU and aminoguanidine neutralized the effect of cadaverine-induced increase in the activity of catalase and guaiacol peroxidase, but had almost no effect on the increase in SOD activity in roots induced by this diamine (See Fig. 6). The NADPH oxidase inhibitor imidazole did not significantly affect the manifestation of the effect of increasing the activity of antioxidant enzymes when seedlings are treated with cadaverine. We can conclude that one of the signaling mediators involved in the regulation activity of catalase and guaiacol peroxidase and in the induction of heat resistance of wheat seedlings by exogenous cadaverine is hydrogen peroxide, which is formed during the oxidation of cadaverine by diamine oxidase. At the same time, the modification of SOD activity in the roots of wheat seedlings with cadaverine, apparently, can occur without the participation of ROS.

Effects of Bile Salt Deconjugation by Probiotic Strains on the Survival of Antibiotic-Resistant Foodborne Pathogens under Simulated Gastric Conditions

2012 ◽  
Vol 75 (6) ◽  
pp. 1090-1098 ◽  
Author(s):  
XINLONG HE ◽  
YUNYUN ZOU ◽  
YOUNGJAE CHO ◽  
JUHEE AHN
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Foodborne Pathogens ◽  
Antibiotic Susceptibility ◽  
High Performance ◽  
Bifidobacterium Longum ◽  
Lactobacillus Rhamnosus ◽  
Antibiotic Resistant ◽  
Study Results ◽  
Probiotic Strains

This study was designed to evaluate the effects of bile acid deconjugation by probiotic strains on the antibiotic susceptibility of antibiotic-sensitive and multiple antibiotic–resistant Salmonella Typhimurium and Staphylococcus aureus. Eight probiotic strains, Bifidobacterium longum B6, Lactobacillus acidophilus ADH, Lactobacillus brevis KACC 10553, Lactobacillus casei KACC 12413, Lactobacillus paracasei ATCC 25598, Lactobacillus rhamnosus GG, Leuconostoc mesenteroides KACC 12312, and Pediococcus acidilactici KACC 12307, were used to examine bile acid tolerance. The ability to deconjugate bile acids was evaluated using both thin-layer chromatography and high-performance liquid chromatography. The antibiotic susceptibility testing was carried out to determine the synergistic inhibitory activity of deconjugated bile acids. L. acidophilus, L. brevis, and P. acidilactici showed the most tolerance to the conjugated bile acids. P. acidilactici deconjugated glycocholic acid and glycodeoxycholate from 3.18 and 3.09 mM to the detection limits, respectively. The antibiotic susceptibility of selected foodborne pathogens was increased by increasing the concentration of deconjugated bile acids. The study results are useful for understanding the relationship between bile acid deconjugation by probiotic strains and antibiotic susceptibility in the presence of deconjugated bile acids, and they may be useful for designing new probiotic-antibiotic combination therapy based on bile acid deconjugation.

scholarly journals Combination of Exercise Training and SOD Mimetic Tempol Enhances Upregulation of Nitric Oxide Synthase in the Kidney of Spontaneously Hypertensive Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Pengyu Cao ◽  
Osamu Ito ◽  
Daisuke Ito ◽  
Rong Rong ◽  
Yang Zheng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Exercise Training ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Sod Activity ◽  
Spontaneously Hypertensive ◽  
Nadph Oxidase Activity ◽  
Expression Levels

Both exercise training (Ex) and superoxide dismutase (SOD) mimetic tempol have antihypertensive and renal protective effects in rodent models of several hypertensions. We recently reported that Ex increases nitric oxide (NO) production and the expression levels of endothelial and neuronal NO synthase (eNOS and nNOS) in the kidney and aorta of the spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto rats (WKY). We also found that endogenous hydrogen peroxide (H2O2) upregulates the expression levels of eNOS and nNOS in SHR. To elucidate the mechanism of the Ex-upregulated NO system in the kidney, we examined the additive effect of Ex and tempol on the renal NO system in SHR and WKY. Our data showed that, in SHR, both Ex and tempol increase the levels of H2O2 and nitrate/nitrite (NOx) in plasma and urine. We also observed an increased renal NOS activity and upregulated expression levels of eNOS and nNOS with decreased NADPH oxidase activity. The effects of the combination of Ex and tempol on these variables were cumulate in SHR. On the other hand, we found that Ex increases these variables with increased renal NADPH oxidase activity, but tempol did not change these variables or affect the Ex-induced upregulation in the activity and expression of NOS in WKY. The SOD activity in the kidney and aorta was activated by tempol only in SHR, but not in WKY; whereas Ex increased SOD activity only in the aorta in both SHR and WKY. These results indicate that Ex-induced endogenous H2O2 produced in the blood vessel and other organs outside of the kidney may be carried to the kidney by blood flow and stimulates the NO system in the kidney.

scholarly journals A Novel H+ Conductance in Eosinophils

1999 ◽  
Vol 190 (2) ◽  
pp. 183-194 ◽  
Author(s):  
Botond Bánfi ◽  
Jacques Schrenzel ◽  
Oliver Nüsse ◽  
Daniel P. Lew ◽  
Erzsébet Ligeti ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
The Novel ◽  
Experimental Conditions ◽  
Intact Cells ◽  
Electrophysiological Studies ◽  
Dependent Signal ◽  
Low Threshold ◽  
Nadph Oxidase Activation ◽  
In Cells

Efficient mechanisms of H+ ion extrusion are crucial for normal NADPH oxidase function. However, whether the NADPH oxidase—in analogy with mitochondrial cytochromes—has an inherent H+ channel activity remains uncertain: electrophysiological studies did not find altered H+ currents in cells from patients with chronic granulomatous disease (CGD), challenging earlier reports in intact cells. In this study, we describe the presence of two different types of H+ currents in human eosinophils. The “classical” H+ current had properties similar to previously described H+ conductances and was present in CGD cells. In contrast, the “novel” type of H+ current had not been described previously and displayed unique properties: (a) it was absent in cells from gp91- or p47-deficient CGD patients; (b) it was only observed under experimental conditions that allowed NADPH oxidase activation; (c) because of its low threshold of voltage activation, it allowed proton influx and cytosolic acidification; (d) it activated faster and deactivated with slower and distinct kinetics than the classical H+ currents; and (e) it was ∼20-fold more sensitive to Zn2+ and was blocked by the histidine-reactive agent, diethylpyrocarbonate (DEPC). In summary, our results demonstrate that the NADPH oxidase or a closely associated protein provides a novel type of H+ conductance during phagocyte activation. The unique properties of this conductance suggest that its physiological function is not restricted to H+ extrusion and repolarization, but might include depolarization, pH-dependent signal termination, and determination of the phagosomal pH set point.

scholarly journals Olfactomedin 4 contributes to hydrogen peroxide-induced NADPH oxidase activation and apoptosis in mouse neutrophils

2018 ◽  
Vol 315 (4) ◽  
pp. C494-C501 ◽  
Author(s):  
Wenli Liu ◽  
Yueqin Liu ◽  
Hongzhen Li ◽  
Griffin P. Rodgers
Keyword(s):  
Hydrogen Peroxide ◽  
Nadph Oxidase ◽  
Molecular Mechanisms ◽  
Oxidase Inhibitor ◽  
Superoxide Production ◽  
Wild Type ◽  
Escherichia Coli Bacteria ◽  
Induced Apoptosis ◽  
Nadph Oxidase Activation ◽  
Deficient Mice

Neutrophils increase production of reactive oxygen species, including superoxide, hydrogen peroxide (H2O2), and hydroxyl radical, to destroy invading microorganisms under pathological conditions. Conversely, oxidative stress conditions, such as the presence of H2O2, induce neutrophil apoptosis, which helps to remove neutrophils after inflammation. However, the detailed molecular mechanisms that are involved in the latter process have not been elucidated. In this study, we investigated the potential role of olfactomedin 4 (Olfm4) in H2O2-induced superoxide production and apoptosis in mouse neutrophils. We have demonstrated that Olfm4 is not required for maximal-dosage PMA- and Escherichia coli bacteria-induced superoxide production, but Olfm4 contributes to suboptimal-dosage PMA- and H2O2-induced superoxide production. Using an NADPH oxidase inhibitor and gp91phox-deficient mouse neutrophils, we found that NAPDH oxidase was required for PMA-stimulated superoxide production and that Olfm4 mediated H2O2-induced superoxide production through NADPH oxidase, in mouse neutrophils. We have shown that neutrophils from Olfm4-deficient mice exhibited reduced H2O2-induced apoptosis compared with neutrophils from wild-type mice. We also demonstrated that neutrophils from Olfm4-deficient mice exhibited reduced H2O2-stimulated mitochondrial damage and membrane permeability, and as well as reduced caspase-3 and caspase-9 activity, compared with neutrophils from wild-type mice. Moreover, the cytoplasmic translocation of the proapoptotic mitochondrial proteins Omi/HtrA2 and Smac/DIABLO in response to H2O2was reduced in neutrophils from Olfm4-deficient mice compared with neutrophils from wild-type mice. Our study demonstrates that Olfm4 contributes to H2O2-induced NADPH oxidase activation and apoptosis in mouse neutrophils. Olfactomedin 4 might prove to be a potential target for future studies on inflammatory neutrophil biology and for inflammatory disease treatment.

Sign in / Sign up

Export Citation Format

Share Document