4.5 Article

Effects of moderate exercise on lipopolysaccharide-induced inflammatory responses in rat's cardiac tissue

Journal

CYTOKINE
Volume 138, Issue -, Pages -

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2020.155409

Keywords

Lipopolysaccharide; Moderate exercise; Cardiac tissue; Cytokine; Apoptosis; Oxidative damage

Funding

  1. Mashhad University of Medical Sciences [971874]

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Moderate exercise can improve the detrimental effects of lipopolysaccharide on cardiac tissue by attenuating proinflammatory cytokine levels, apoptosis, and oxidative damage to protect heart health.
The effects of moderate exercise on cardiac tissue inflammation, oxidative stress markers and apoptosis in lipopolysaccharide (LPS)-administered rats were evaluated. Wistar rats were divided into three groups (N = 8): (1) control; (2) LPS (1 mg/kg); and (3) LPS + moderate training (LPS + EX: 15 m/min, 30 min/day, for 9 weeks (week 1-9)). LPS was injected intraperitoneally for 5 days during week 9. Finally, the rats' heart were removed for biochemical and expression assessments. LPS increased the levels of tumor necrosis factor alpha (TNF-alpha), interleukin (IL)1 beta, C-reactive protein (CRP), malondialdehyde (MDA) and nitric oxide (NO) metabolites in cardiac tissue, but decreased thiol contents and catalase (CAT) and superoxide dismutase (SOD) activity in cardiac tissue compared to the control group (p < 0.05-p < 0.001). In LPS + EX group, the level of NO metabolites was increased (p < 0.05) and thiol contents were decreased (p < 0.001) compared to the control group. Moderate training decreased the levels of TNF-alpha, IL-1 beta, CRP and NO metabolites while increased CAT activity in the LPS + EX group compared to the LPS group (p < 0.05-p < 0.001). The mRNA level of BAX in the LPS group and the BCL2/BAX ratio in both LPS and LPS + EX groups increased compared to the control group (p < 0.05-p < 0.01). These results indicated that moderate training improved LPS-induced deleterious effects on cardiac tissue by attenuating proinflammatory cytokine levels, apoptosis and oxidative damage.

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