Moderate swimming exercise and caffeine supplementation reduce the levels of inflammatory cytokines without causing oxidative stress in tissues of middle-aged rats

Amino Acids ◽  
2014 ◽  
Vol 46 (5) ◽  
pp. 1187-1195 ◽  
Author(s):  
José L. Cechella ◽  
Marlon R. Leite ◽  
Fernando Dobrachinski ◽  
Juliana T. da Rocha ◽  
Nelson R. Carvalho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Swimming Exercise ◽  
Aged Rats ◽  
Middle Aged

scholarly journals Early Hepatic Oxidative Stress and Mitochondrial Changes Following Western Diet in Middle Aged Rats

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2670 ◽  
Author(s):  
Arianna Mazzoli ◽  
Raffaella Crescenzo ◽  
Luisa Cigliano ◽  
Maria Stefania Spagnuolo ◽  
Rosa Cancelliere ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Dietary Habits ◽  
Western Diet ◽  
Hepatic Insulin Resistance ◽  
Whole Body ◽  
Myeloperoxidase Activity ◽  
Aged Rats ◽  
Middle Aged ◽  
Markers Of Oxidative Stress

To assess the effect of 4 weeks of high fat-high fructose feeding on whole body composition, energy balance, specific markers of oxidative stress and inflammation, and insulin sensitivity in the liver of middle-aged rats, rats (1 year) were fed a diet rich in saturated fatty acids and fructose (HFF rats), mimicking the “Western diet”, and compared with rats of the same age that were fed a low fat diet (LF rats). HFF rats exhibited a significant increase in the gain of body weight, energy, and lipids compared to LF rats. HFF rats also showed hepatic insulin resistance, together with an increase in plasma triglycerides, cholesterol, and tumor necrosis factor alpha. Hepatic lipids, triglycerides and cholesterol were higher in HFF rats, while a significant decrease in Stearoyl-CoA desaturase activity was found in this tissue. A marked increase in the protein amount of complex I, concomitant to a decrease in its contribution to mitochondrial respiration, was found in HFF rats. Lipid peroxidation and Nitro-Tyrosine content, taken as markers of oxidative stress, as well as NADPH oxidase activity, were significantly higher in HFF rats, while the antioxidant enzyme catalase decreased in these rats. Myeloperoxidase activity and lipocalin content increased, while peroxisome proliferator activated receptor gamma decreased in HFF rats. The present results provide evidence that middle-aged rats show susceptibility to a short-term “Western diet”, exhibiting altered redox homeostasis, insulin resistance, and early mitochondrial alterations in the liver. Therefore, this type of dietary habits should be drastically limited to pursue a “healthy aging”.

P2253Intake of the omega 3 PUFAs formulation EPA:DHA 6:1 by aged rats reduced shedding of microvesicles from spleen-derived cultured leukocytes and their ability to promote senescence in endothelial cells

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A W Qureshi ◽  
R Altamimy ◽  
A El Habhab ◽  
L Amoura ◽  
S Khemais-Berkhiat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Inflammatory Responses ◽  
Premature Senescence ◽  
Aged Rats ◽  
Omega 3 ◽  
Middle Aged ◽  
Angiotensin System ◽  
Coronary Syndrome

Abstract Introduction Ageing is associated with the appearance of endothelial senescence promoting endothelial dysfunction and, ultimately, cardiovascular events. Circulating microvesicles (MVs) of patients with acute coronary syndrome promoted premature endothelial senescence by stimulating the local angiotensin system. Omega 3 PUFAs have been shown to reduce the risk of cardiovascular disease in patients at high risk. Purpose This study investigated whether a 7-day intake of the omega 3 formulation EPA:DHA 6:1 by rats affects the level of MVs released by spleen-derived cultured leukocytes as well as their ability to promote premature senescence in target endothelial cells (ECs), and, if so, to clarify the underlying mechanism. Methods Middle-aged male Wistar rats (M, 48-week old) received 500 mg/kg/d of either EPA:DHA 6:1, EPA:DHA 1:1, or vehicle (CTL) for 7 days. Thereafter, spleen-derived leukocytes, a rich source of MVs, were prepared and cultured for 24 h. Cultured ECs were prepared from porcine coronary arteries. Senescence-associated β-galactosidase activity (SA-β-gal) was assessed by C12FDG, protein expression level by Western blot analysis, oxidative stress by dihydroethidium using confocal microscopy, and procoagulant MVs by prothrombinase assay. Spleen-derived leukocytes from untreated young (Y, 12-week) and old (O, 72-week) rats were also studied. Results Shedding of MVs by spleen-derived leukocytes significantly increased with increasing age. Incubation of ECs with leukocyte-derived MVs (10 nM Phtd Ser eq.) from M and O but not those from Y induced premature senescence after 48 h. The stimulatory effect of M-MVs was prevented by losartan and associated with oxidative stress. M-MVs induced an upregulation of senescence markers (p16, p21, p53), pro-atherothrombotic markers (VCAM-1, ICAM-1, tissue factor), the pro-inflammatory marker cyclooxygenase-2 (COX-2) but not COX-1, and of the angiotensin system (angiotensin-converting enzyme and type 1 angiotensin receptor), whereas endothelial NO synthase was down-regulated. A one-week intake of EPA:DHA 1:1 and 6:1 by M rats decreased the leukocyte-derived MVs shedding by about 14% and 24%, and EPA:DHA 6:1 reduced their ability to induce ECs senescence by 38%. The stimulatory effect of M-MVs on the expression of target proteins was also observed with those from the EPA:DHA 1:1 but not with those from the 6:1 group. Conclusion These findings indicate that ingestion of EPA:DHA 6:1 by middle-aged rats reduces not only the shedding of MVs by spleen-derived leukocytes but also their ability to induce pro-senescent, pro-thrombotic and pro-inflammatory responses in endothelial cells most likely by decreasing the local angiotensin system. They further suggest that EPA:DHA 6:1 may help to delay ageing-related endothelial dysfunction. Acknowledgement/Funding Unrestricted research grant from PIVOTAL Therapeutics Inc.

Grape seed proanthocyanidin lowers brain oxidative stress in adult and middle-aged rats

2011 ◽  
Vol 46 (11) ◽  
pp. 958-964 ◽  
Author(s):  
S. Asha Devi ◽  
B.K. Sagar Chandrasekar ◽  
K.R. Manjula ◽  
N. Ishii
Keyword(s):  
Oxidative Stress ◽  
Grape Seed ◽  
Aged Rats ◽  
Middle Aged ◽  
Brain Oxidative Stress ◽  
Grape Seed Proanthocyanidin

Protective Effects of Exercise Training Against Aged Induced the Reduction of Cardiac Angiogenic Capacity in Middle Aged Rats

2020 ◽  
Vol 04 (01) ◽  
Author(s):  
Titiporn Mekrungruangwong ◽  
Pimpetch Kasetsuwan ◽  
Sheepsumon Viboolvorakul ◽  
Suthiluk Patumraj
Keyword(s):  
Exercise Training ◽  
Protective Effects ◽  
Aged Rats ◽  
Middle Aged

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

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