scholarly journals Dietary Strawberries Improve Biomarkers of Antioxidant Status and Endothelial Function in Adults with Cardiometabolic Risks in a Randomized Controlled Crossover Trial

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1730
Author(s):  
Arpita Basu ◽  
Kenneth Izuora ◽  
Nancy M. Betts ◽  
Jeffrey L. Ebersole ◽  
Robert Hal Scofield
Keyword(s):  
Endothelial Function ◽  
Antioxidant Status ◽  
Vegetable Intake ◽  
High Dose ◽  
Randomized Controlled ◽  
Cardiometabolic Risks ◽  
Factor Α ◽  
Study Participants ◽  
Cell Adhesion Molecule 1 ◽  
Necrosis Factor

Strawberries, a popularly consumed berry fruit, are rich in bioactive compounds with antioxidant effects. In this study, we examined the effects of two dietary achievable doses of strawberries on the antioxidant status and biomarkers of endothelial function in adults with features of metabolic syndrome and a confirmed low baseline of fruit and vegetable intake. In a 14-week randomized controlled crossover study, participants were assigned to one of three groups for four weeks separated by a one-week washout period: control powder, one serving (low dose: 13 g strawberry powder/day), or 2.5 servings (high dose: 32 g strawberry powder/day). Blood samples and health data were collected at baseline and at the end of each four-week phase of intervention. Thirty-three participants completed all three phases of the trial. Significant increases were observed in serum antioxidant capacity and superoxide dismutase activity as well as decreases in lipid peroxidation after both low and high dose strawberry phases when compared with the control phase. Significant decreases were also observed in soluble vascular cell adhesion molecule-1 and tumor necrosis factor-α with the high dose strawberry phase. These data confirm that consuming strawberries for four weeks significantly improves antioxidant status, endothelial function, and inflammation in adults with cardiometabolic risks.

scholarly journals Inhibition of TNF-α production contributes to the attenuation of LPS-induced hypophagia by pentoxifylline

2000 ◽  
Vol 279 (6) ◽  
pp. R2113-R2120 ◽  
Author(s):  
M. H. Porter ◽  
B. J. Hrupka ◽  
G. Altreuther ◽  
M. Arnold ◽  
W. Langhans
Keyword(s):  
Bacterial Infections ◽  
Tumor Necrosis ◽  
Low Dose ◽  
Potent Inhibitor ◽  
Muramyl Dipeptide ◽  
High Dose ◽  
Tnf Α ◽  
Anorectic Effect ◽  
Factor Α ◽  
Necrosis Factor

Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are assumed to mediate anorexia during bacterial infections. To improve our understanding of the role that these two cytokines serve in mediating infection during anorexia, we investigated the ability of pentoxifylline (PTX), a potent inhibitor of TNF-α production, to block the anorectic effects of the bacterial products lipopolysaccharide (LPS) and muramyl dipeptide (MDP) in rats. Intraperitoneally injected PTX (100 mg/kg body wt) completely eliminated the anorectic effect of intraperitoneally injected LPS (100 μg/kg body wt) and attenuated the anorectic effect of a higher dose of intraperitoneally injected LPS (250 μg/kg body wt). Concurrently, PTX pretreatment suppressed low-dose LPS-induced TNF-α production by more than 95% and IL-1β production 39%, as measured by ELISA. Similarly, high-dose LPS-induced TNF-α production was reduced by ∼90%. PTX administration also attenuated the tolerance that is normally observed with a second injection of LPS. In addition, PTX pretreatment attenuated the hypophagic effect of intraperitoneally injected MDP (2 mg/kg body wt) but had no effect on the anorectic response to intraperitoneally injected recombinant human TNF-α (150 ug/kg body wt). The results suggest that suppression of TNF-α production is sufficient to attenuate LPS- and MDP-induced anorexia. This is consistent with the hypothesis that TNF-α plays a major role in the anorexia associated with bacterial infection.

scholarly journals Tumor Necrosis Factor α-Induced Eosinophil Accumulation in Rat Skin Is Dependent on α4 Integrin/Vascular Cell Adhesion Molecule-1 Adhesion Pathways

Blood ◽  
1997 ◽  
Vol 90 (10) ◽  
pp. 4144-4152 ◽  
Author(s):  
Maria-Jesus Sanz ◽  
Adele Hartnell ◽  
Patricia Chisholm ◽  
Cindy Williams ◽  
Dawn Davies ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Cell Adhesion Molecule ◽  
Tumor Necrosis Factor Α ◽  
Vascular Cell Adhesion ◽  
Rat Skin ◽  
Vascular Cell ◽  
Factor Α ◽  
Cell Adhesion Molecule 1 ◽  
Necrosis Factor ◽  
Eosinophil Accumulation

Abstract Tumor necrosis factor α (TNFα) is a cytokine implicated in the pathogenesis of numerous chronic and acute inflammatory conditions. In the present study, we have characterized the ability of TNFα in inducing eosinophil accumulation in rat skin and have shown the inhibitory effects of anti-α4 integrin and anti–vascular cell adhesion molecule-1 (VCAM-1) antibodies on this response. The intradermal injection of recombinant human TNFα induced a slowly developing, dose-dependent accumulation of 111In-eosinophils in rat skin that was maximal at the dose of 10−11 mol/site. Coadministration of TNFα with the soluble TNFα receptor (p55)-IgG fusion protein (TNFR-IgG) totally inhibited the 111In-eosinophil accumulation induced by the cytokine. The TNFα-induced 111In-eosinophil accumulation was not affected after pretreatment of rats with the platelet-activating factor (PAF) receptor antagonist UK-74,505 or the antihuman interleukin-8 monoclonal antibody (MoAb) DM/C7. In contrast, the intravenous administration of an anti-α4 integrin MoAb, HP2/1 (3.5 mg/kg), or an anti–VCAM-1 MoAb, 5F10 (2 mg/kg), greatly inhibited the 111In-eosinophil accumulation induced by TNFα (the responses detected at 10−11 mol/site were inhibited by 78% and 50%, respectively). These results show that TNFα is an effective inducer of eosinophil accumulation in vivo, with this response being dependent on an interaction between α4 integrins and VCAM-1.

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