In vitro effects of peanut skin polyphenolic extract on oxidative stress, adipogenesis and lipid accumulation

2021 ◽  
Author(s):  
Annayara C. F. Fernandes ◽  
Ádina L. Santana ◽  
Natália C. Vieira ◽  
Renata L. P. Gandra ◽  
Camila Rubia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
Peanut Skin ◽  
Polyphenolic Extract ◽  
In Vitro Effects

scholarly journals Aminoguanidine Protects Boar Spermatozoa against the Deleterious Effects of Oxidative Stress

Pharmaceutics ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 212 ◽  
Author(s):  
Eliana Pintus ◽  
Martin Kadlec ◽  
Marija Jovičić ◽  
Markéta Sedmíková ◽  
José Ros-Santaella
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Antioxidant Properties ◽  
In Vitro Effects ◽  
Oxide Synthase ◽  
Boar Spermatozoa ◽  
Generating System ◽  
Control Samples ◽  
Inducible Nitric Oxide

Aminoguanidine is a selective inhibitor of the inducible nitric oxide synthase (iNOS) and a scavenger of reactive oxygen species (ROS). Numerous studies have shown the antioxidant properties of aminoguanidine in several cell lines, but the in vitro effects of this compound on spermatozoa under oxidative stress are unknown. In this study, we tested the hypothesis that aminoguanidine may protect against the detrimental effects of oxidative stress in boar spermatozoa. For this purpose, sperm samples were incubated with a ROS generating system (Fe2+/ascorbate) with or without aminoguanidine supplementation (10, 1, and 0.1 mM). Our results show that aminoguanidine has powerful antioxidant capacity and protects boar spermatozoa against the deleterious effects of oxidative stress. After 2 h and 3.5 h of sperm incubation, the samples treated with aminoguanidine showed a significant increase in sperm velocity, plasma membrane and acrosome integrity together with a reduced lipid peroxidation in comparison with control samples (p < 0.001). Interestingly, except for the levels of malondialdehyde, the samples treated with 1 mM aminoguanidine did not differ or showed better performance than control samples without Fe2+/ascorbate. The results from this study provide new insights into the application of aminoguanidine as an in vitro therapeutic agent against the detrimental effects of oxidative stress in semen samples.

The In Vitro Effects of Propofol on Tissular Oxidative Stress in the Rat

1998 ◽  
Vol 87 (5) ◽  
pp. 1141-1146 ◽  
Author(s):  
J. P. De La Cruz ◽  
G. Sedeno ◽  
J. A. Carmona ◽  
F. Sanchez de la Cuesta
Keyword(s):  
Oxidative Stress ◽  
In Vitro Effects

In vitro effects of NSAIDS and paracetamolon oxidative stress-related parameters of human erythrocytes

2001 ◽  
Vol 53 (2-3) ◽  
pp. 133-140 ◽  
Author(s):  
Hilmi Orhan ◽  
Gönül Şahin
Keyword(s):  
Oxidative Stress ◽  
Human Erythrocytes ◽  
In Vitro Effects

Differential in vitro effects of homoarginine on oxidative stress in plasma, erythrocytes, kidney and liver of rats in the absence and in the presence α-tocopherol, ascorbic acid or L-NAME

Amino Acids ◽  
2015 ◽  
Vol 47 (9) ◽  
pp. 1931-1939 ◽  
Author(s):  
Simone Sasso ◽  
Leticia Dalmedico ◽  
Débora Delwing-Dal Magro ◽  
Eduardo Manoel Pereira ◽  
Angela T. S. Wyse ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
In Vitro Effects

2288Oxidized LDL/CD36/PPARg circuitry is a trigger of adipogenesis in arrhythmogenic cardiomyopathy

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Stadiotti ◽  
E Sommariva ◽  
M Casella ◽  
V Catto ◽  
A Dello Russo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
Foam Cell ◽  
Plasma Cholesterol ◽  
Foam Cell Formation ◽  
Arrhythmogenic Cardiomyopathy ◽  
Knock Out ◽  
Fatty Replacement

Abstract Background Arrhythmogenic Cardiomyopathy (ACM) is a genetic condition hallmarked by ventricular fibro-fatty replacement and arrhythmias. Cardiac mesenchymal stromal cells (C-MSC) differentiate into adipocytes in ACM hearts, through the activation of PPARγ, caused by ACM mutations (e.g. PKP2). The clinical phenotype of ACM is variable for poorly understood reasons. The only recognized cofactor is physical exercise, which is known to increases oxidative stress. An accepted marker of exercise-induced oxidative stress is 13HODE, a component of oxLDL and direct activator of PPARγ. In macrophages, during foam cell formation, 13HODE creates a feed-forward loop increasing both PPARγ and the oxLDL receptor CD36, resulting in fat accumulation. Purpose To investigate oxLDL effects on ACM adipogenesis and to dissect the involved pathways. Methods We analyzed plasmas (n=42) and ventricular tissues (n=4) of ACM patients and matched healthy controls (HC). For in vitro experiments, ACM and HC C-MSC (n=10) have been used, while in vivo experiments have been conducted in heterozygous Pkp2 knock-out mice (Pkp2+/−; n=10). Results We observed higher plasma oxLDL in ACM patients compared to HC (ACM 246.70±55.89 vs HC 102.5±17.95ng/ml; p=0.019). oxLDL levels also discriminate between ACM patients with overt phenotype and their unaffected relatives carriers of the same causative mutations (p=0.03). We observed higher oxidative stress (MDA intensity 40.87±11.76 fold; p=0.015) and CD36 levels (14.72±2.10 fold; p=0.0007) in ACM ventricular tissue, compared to HC. In basal conditions, ACM C-MSC showed greater oxidative stress (MDA intensity 8.83±2.78 fold p=0.017) and higher expression of PPARγ (1.47±0.14 fold; p=0.009) compared to HC C-MSC. The adipogenic stimulation led to a parallel increase of CD36 and lipid accumulation, mainly in ACM C-MSC (slopes statistically different p=0.016). OxLDL and 13HODE administration increased lipid accumulation in ACM C-MSC (ORO staining ACM vs ACM+oxLDL p=0.01; ACM vs ACM+13HODE p=0.014). On the contrary, the antioxidant N-Acetylcysteine (NAC) prevented lipid accumulation in ACM C-MSC (ORO staining ACM+13HODE vs ACM+13HODE+NAC p=0.0009). Through CD36 silencing of ACM C-MSC, we obtained a significantly lower lipid accumulation than non-silenced cells (ORO staining 0.35±0.10 fold; p=0.003). Pkp2+/− mice do not spontaneously accumulate adipocytes in the heart, however Pkp2+/− C-MSC are more prone to lipid accumulation in vitro than WT cells (p=0.007). Accordingly, mice have low plasma oxLDL and cardiac oxidative stress. By increasing plasma cholesterol and oxidative stress through high fat diet, we observed fibro-fatty substitution in Pkp2+/− hearts (p=0.046). Figure 1 Conclusions These findings reveal a modulatory role of oxidized lipids in ACM adipogenesis at a cellular, tissue and clinical level, enlightening novel targets for pharmacological strategies to prevent adipogenic substitution and consequent ACM clinical phenotypes. Acknowledgement/Funding Telethon Foundation; Italian Ministry of Health

scholarly journals The Nutraceutic Silybin Counteracts Excess Lipid Accumulation and Ongoing Oxidative Stress in an In Vitro Model of Non-Alcoholic Fatty Liver Disease Progression

2017 ◽  
Vol 4 ◽  
Author(s):  
Giulia Vecchione ◽  
Elena Grasselli ◽  
Federica Cioffi ◽  
Francesca Baldini ◽  
Paulo J. Oliveira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
In Vitro Model ◽  
Alcoholic Fatty Liver ◽  
Liver Disease Progression ◽  
Vitro Model ◽  
Alcoholic Fatty Liver Disease

In vivo and in vitro effects of SREBP-1 on diabetic renal tubular lipid accumulation and RNAi-mediated gene silencing study

2008 ◽  
Vol 131 (3) ◽  
pp. 327-345 ◽  
Author(s):  
Hao Jun ◽  
Zhao Song ◽  
Wang Chen ◽  
Rong Zanhua ◽  
Shi Yonghong ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Lipid Accumulation ◽  
In Vitro Effects ◽  
Renal Tubular
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