Ceratonia siliqua leaves exert a strong ROS-scavenging effect in human neutrophils, inhibit myeloperoxydase in vitro and protect against intestinal fluid and electrolytes secretion in rats

RSC Advances ◽  
2016 ◽  
Vol 6 (70) ◽  
pp. 65483-65493 ◽  
Author(s):  
Kaïs Rtibi ◽  
Mohammed-Amine Jabri ◽  
Slimen Selmi ◽  
Hichem Sebai ◽  
Mohamed Amri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Neutrophils ◽  
Physical Factors ◽  
Ceratonia Siliqua ◽  
Intestinal Fluid ◽  
Ros Scavenging ◽  
Scavenging Effect ◽  
Increased Risk ◽  
And Oxidative Stress

Chronic inflammation and oxidative stress are induced by biological, chemical and physical factors which are, in turn, associated with an increased risk of several human diseases.

scholarly journals Coenzyme Q10, Ageing and the Nervous System: An Overview

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 2
Author(s):  
David Mantle ◽  
Robert A. Heaton ◽  
Iain P. Hargreaves
Keyword(s):  
Oxidative Stress ◽  
Coenzyme Q10 ◽  
Neurological Disorders ◽  
Neurological Disease ◽  
Age Related ◽  
Increased Risk ◽  
Potential Therapeutic Role ◽  
Ageing Brain ◽  
And Oxidative Stress

The ageing brain is characterised by changes at the physical, histological, biochemical and physiological levels. This ageing process is associated with an increased risk of developing a number of neurological disorders, notably Alzheimer’s disease and Parkinson’s disease. There is evidence that mitochondrial dysfunction and oxidative stress play a key role in the pathogenesis of such disorders. In this article, we review the potential therapeutic role in these age-related neurological disorders of supplementary coenzyme Q10, a vitamin-like substance of vital importance for normal mitochondrial function and as an antioxidant. This review is concerned primarily with studies in humans rather than in vitro studies or studies in animal models of neurological disease. In particular, the reasons why the outcomes of clinical trials supplementing coenzyme Q10 in these neurological disorders is discussed.

1 INSULIN TREATMENT DURING IN VITRO OOCYTE MATURATION LEADS TO DIFFERENT GENE EXPRESSION AND METHYLATION PATTERNS OF KEY GENES ASSOCIATED WITH METABOLISM AND STEROID SYNTHESIS IN THE BOVINE BLASTOCYST

2017 ◽  
Vol 29 (1) ◽  
pp. 108
Author(s):  
D. Laskowski ◽  
P. Humblot ◽  
M. A. Sirard ◽  
Y. Sjunnesson ◽  
G. Andersson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Oocyte Maturation ◽  
Steroid Synthesis ◽  
Developmental Potential ◽  
Increased Risk ◽  
In Vitro Oocyte Maturation ◽  
Methylation Patterns ◽  
And Oxidative Stress

Obesity and overfeeding are common causes for female infertility, leading to insulin resistance and hyperinsulinemia and associated with an increased risk for type 2 diabetes mellitus (Pasquali et al., http://dx.doi.org/10.1093/humupd/dmg024). We investigated here the effect of insulin during in vitro oocyte maturation on methylation changes in bovine Day 8 blastocysts (BC8) and focused on methylation patterns of candidate genes associated with metabolism and steroidogenesis (Day 0 = day of oocyte collection). Abattoir-derived oocytes (n = 882) were in vitro matured for 22 h with 2 different insulin concentrations, INS10 (10 µg mL−1) and INS0.1 (0.1 µg mL−1) or without insulin (INS0, control). Subsequently, IVF and IVC were performed to equal standardized conditions for all groups. Parallel genomic DNA and total RNA extraction (AllPrepDNA/RNA micro kit, cat no. 80284, Qiagen®, Valencia, CA, USA) from pools of 10 frozen (−80°C) BC8 was followed by transcriptome and epigenome analysis (Laskowski et al., http://dx.doi.org/10.1071/RD15315). An empirical Bayes moderated t-test and the ‘limma’ package in R (www.r-project.org) were used to search for differentially expressed genes between the control and the insulin groups. Analysis of the epigenome by using a specific pipeline, described by Shojaei Saadi et al. (2014 BMC Genomics 15, 451), showed that 7632 and 3914 regions were hypomethylated in the INS0.1 and INS10 v. INS0, whereas 6026 and 8504 regions were hypermethylated in INS0.1 and INS10 v. INS0. Combining epigenetic and transcriptomic data, we found that high methylation and low expression or the reverse (low methylation and high expression) were observed for a set of 14 and 11 genes for INS0.1 and INS10 respectively. Most of these genes are associated with lipid metabolism, steroid synthesis, and oxidative stress. Further investigation of the localization of differentially methylated regions (DMR) in genes showed that the conservation odds (methylation) was in general higher in coding regions and CpG islands than in noncoding regions. We observed a large overlap of DMR in the 2 insulin groups compared with controls (3233 common DMR). These numerous changes illustrate the potential unfavourable effects of elevated insulin during maturation leading to alteration of the methylation patterns of the early embryo. This model may help us better understand the mechanisms by which metabolic disorders observed pre-conception can affect embryonic development and subsequent health of the offspring. Our results based on changes in transcriptome or epigenome did show that insulin challenge during maturation leads to postponed effects associated with steroidogenesis, lipid metabolism and oxidative stress in the BC8. By this early stage, if persistent, specific changes in the expression and methylation patterns of genes associated to hyperinsulinemia may decrease the developmental potential of early embryos or could be responsible for subsequent pathologies. This study was funded by FORMAS.

Carob pods (Ceratonia siliqua L.) inhibit human neutrophils myeloperoxidase and in vitro ROS-scavenging activity

RSC Advances ◽  
2015 ◽  
Vol 5 (102) ◽  
pp. 84207-84215 ◽  
Author(s):  
Kaïs Rtibi ◽  
Mohamed Amine Jabri ◽  
Slimen Selmi ◽  
Abdelaziz Souli ◽  
Hichem Sebai ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Human Neutrophils ◽  
Scavenging Activity ◽  
Ceratonia Siliqua ◽  
Ros Scavenging ◽  
Ceratonia Siliqua L ◽  
Chromatographic Profiles

Chromatographic profiles of aqueous extract of carob pods ((A) pulp and (B) seeds).

scholarly journals Hypoxia and oxidative stress induce sterile placental inflammation in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bernadette C. Baker ◽  
Alexander E. P. Heazell ◽  
Colin Sibley ◽  
Rachael Wright ◽  
Helen Bischof ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Placental Tissue ◽  
Nitrative Stress ◽  
Increased Risk ◽  
Cell Free Fetal Dna ◽  
Placental Inflammation ◽  
Inflammatory Profile ◽  
Conditioned Culture Medium ◽  
And Oxidative Stress

AbstractFetal growth restriction (FGR) and stillbirth are associated with placental dysfunction and inflammation and hypoxia, oxidative and nitrative stress are implicated in placental damage. Damage-associated molecular patterns (DAMPs) are elevated in pregnancies at increased risk of FGR and stillbirth and are associated with increase in pro-inflammatory placental cytokines. We hypothesised that placental insults lead to release of DAMPs, promoting placental inflammation. Placental tissue from uncomplicated pregnancies was exposed in vitro to hypoxia, oxidative or nitrative stress. Tissue production and release of DAMPs and cytokines was determined. Oxidative stress and hypoxia caused differential release of DAMPs including uric acid, HMGB1, S100A8, cell-free fetal DNA, S100A12 and HSP70. After oxidative stress pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-8, TNFα, CCL2) were increased both within explants and in conditioned culture medium. Hypoxia increased tissue IL-1α/β, IL-6, IL-8 and TNFα levels, and release of IL-1α, IL-6 and IL-8, whereas CCL2 and IL-10 were reduced. IL1 receptor antagonist (IL1Ra) treatment prevented hypoxia- and oxidative stress-induced IL-6 and IL-8 release. These findings provide evidence that relevant stressors induce a sterile inflammatory profile in placental tissue which can be partially blocked by IL1Ra suggesting this agent has translational potential to prevent placental inflammation evident in FGR and stillbirth.

scholarly journals In vitro and in vivo modulation of NADPH-oxidase activity and reactive oxygen species production in human neutrophils by alpha-1 antitrypsin

2021 ◽  
pp. 00234-2021
Author(s):  
Padraig Hawkins ◽  
Thomas McEnery ◽  
Claudie Gabillard-Lefort ◽  
David A Bergin ◽  
Bader Alfawaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Membrane ◽  
Nadph Oxidase ◽  
Ex Vivo ◽  
Human Neutrophils ◽  
Driving Mechanism ◽  
Increased Risk ◽  
Alpha 1 Antitrypsin

Oxidative stress from innate immune cells is a driving mechanism that underlies COPD pathogenesis. Individuals with alpha-1 antitrypsin (AAT) deficiency (AATD) have a dramatically increased risk of developing COPD. To understand this further, the aim of this study was to investigate whether AATD presents with altered neutrophil NADPH-oxidase activation, due to the specific lack of plasma AAT. Experiments were performed using circulating neutrophils isolated from healthy controls and individuals with AATD. Superoxide anion (O2−) production was determined from the rate of reduction of cytochrome c. Quantification of membrane NADPH-oxidase subunits was performed by mass spectrometry and western blot analysis. The clinical significance of our in vitro findings were assessed in patients with AATD and severe COPD receiving intravenous AAT replacement therapy. In vitro, AAT significantly inhibited O2− production by stimulated neutrophils and suppressed receptor stimulation of cyclic adenosimonophosphate (cAMP) and extracellular-signal regulated kinase (ERK)1/2 phosphorylation. In addition, AAT reduced plasma membrane translocation of cytosolic phox components of the NADPH-oxidase. Ex vivo, AATD neutrophils demonstrated increased plasma membrane associated p67phox and p47phox and significantly increased O2− production. The described variance in phox protein membrane assembly was resolved post AAT augmentation therapy in vivo, the effects of which significantly reduced AATD neutrophil O2− production to that of healthy control cells. These results expand our knowledge on the mechanism of neutrophil driven airways disease associated with AATD. Therapeutic AAT augmentation modified neutrophil NADPH-oxidase assembly and ROS production, with implications for clinical use in conditions in which oxidative stress plays a pathogenic role.

scholarly journals Impact of Polyphenolic-Food on Longevity: An Elixir of Life. An Overview

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 507
Author(s):  
Rosaria Meccariello ◽  
Stefania D’Angelo
Keyword(s):  
Oxidative Stress ◽  
Food Sources ◽  
Preventive Action ◽  
Nutritional Interventions ◽  
Beneficial Effects ◽  
Age Related ◽  
Macromolecular Damage ◽  
And Oxidative Stress

Aging and, particularly, the onset of age-related diseases are associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Recently, growing interest has emerged on the beneficial effects of plant-based diets for the prevention of chronic diseases including obesity, diabetes, and cardiovascular disease. Several studies collectively suggests that the intake of polyphenols and their major food sources may exert beneficial effects on improving insulin resistance and related diabetes risk factors, such as inflammation and oxidative stress. They are the most abundant antioxidants in the diet, and their intake has been associated with a reduced aging in humans. Polyphenolic intake has been shown to be effective at ameliorating several age-related phenotypes, including oxidative stress, inflammation, impaired proteostasis, and cellular senescence, both in vitro and in vivo. In this paper, effects of these phytochemicals (either pure forms or polyphenolic-food) are reviewed and summarized according to affected cellular signaling pathways. Finally, the effectiveness of the anti-aging preventive action of nutritional interventions based on diets rich in polyphenolic food, such as the diets of the Blue zones, are discussed.

scholarly journals Uremic Toxins and Their Relation with Oxidative Stress Induced in Patients with CKD

2021 ◽  
Vol 22 (12) ◽  
pp. 6196
Author(s):  
Anna Pieniazek ◽  
Joanna Bernasinska-Slomczewska ◽  
Lukasz Gwozdzinski
Keyword(s):  
Oxidative Stress ◽  
Uremic Toxins ◽  
Water Medium ◽  
Induce Insulin Resistance ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Stage Renal Disease ◽  
End Stage

The presence of toxins is believed to be a major factor in the development of uremia in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Uremic toxins have been divided into 3 groups: small substances dissolved in water, medium molecules: peptides and low molecular weight proteins, and protein-bound toxins. One of the earliest known toxins is urea, the concentration of which was considered negligible in CKD patients. However, subsequent studies have shown that it can lead to increased production of reactive oxygen species (ROS), and induce insulin resistance in vitro and in vivo, as well as cause carbamylation of proteins, peptides, and amino acids. Other uremic toxins and their participation in the damage caused by oxidative stress to biological material are also presented. Macromolecules and molecules modified as a result of carbamylation, oxidative stress, and their adducts with uremic toxins, may lead to cardiovascular diseases, and increased risk of mortality in patients with CKD.

Pirfenidone mediates cigarette smoke extract induced inflammation and oxidative stress in vitro and in vivo

2021 ◽  
Vol 96 ◽  
pp. 107593
Author(s):  
Yiming Ma ◽  
Lijuan Luo ◽  
Xiangming Liu ◽  
Herui Li ◽  
Zihang Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
And Oxidative Stress

In vitro study on the effects of iron sucrose, ferric gluconate and iron dextran on redox-active iron and oxidative stress

2011 ◽  
Vol 60 (07) ◽  
pp. 459-465
Author(s):  
Brigitte Sturm ◽  
Hannes Steinkellner ◽  
Nina Ternes ◽  
Hans Goldenberg ◽  
Barbara Scheiber-Mojdehkar
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Iron Sucrose ◽  
Vitro Study ◽  
Iron Dextran ◽  
Active Iron ◽  
Redox Active ◽  
And Oxidative Stress

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

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