Aim: In the present study, we attempted to investigate whether aerobic exercise could prevent sepsis and its complications and explored the related mechanisms.
Methods: Forty ICR mice were divided into four groups: control (Con), LPS, exercise (Ex), and exercise + LPS (Ex + LPS). Low-intensity aerobic exercise was performed for 4 weeks. Forty-eight hours after the last exercise intervention, LPS and Ex+LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. This study examined the effects of a 4-week exercise pretreatment on LPS-induced changes in blood glucose (BG) levels; inflammatory cytokine levels in BALF; bronchoalveolar lavage fluid (BALF) cell counts; the degree of pulmonary edema; neutrophil density in liver, lung, and kidney tissues; and the gene expression levels of IL-1RN, IL-8, IL-10, TNF-α, Sirt-1, and Nrf-2 in lung tissue. Sixty mice were used to perform survival rate analysis.
Results: A 4-week exercise pretreatment significantly reversed the histopathological severity of LPS-induced lung, heart, liver, kidney, and aortic injuries (P < 0.05) and ameliorated neutrophil inflammation in the lung, heart, liver, and kidney (P < 0.05). A 4-week exercise pretreatment improved survival rates (P < 0.01), deranged glucose homeostasis (P < 0.01), and pulmonary edema (P < 0.01) in mice with sepsis. A 4-week exercise pretreatment increased the levels of IL-6 (P < 0.05), IL-10 (P < 0.05), and IL-1RN (P < 0.05) and decreased the levels of IL-8 (P < 0.05) and TNF-α (P < 0.05) in BALF. A 4-week exercise pretreatment decreased the gene expression levels of IL-8 (P < 0.01) and TNF-α (P < 0.01) and increased the gene expression levels of IL-1RN (P < 0.01) and IL-10 (P < 0.01) in mice with sepsis. 4-week exercise pretreatment activated the gene expression levels of lung protective factors Sirt-1 (P < 0.01) and Nrf-2 (P < 0.01).
Conclusion: Aerobic exercise improved survival rates, multiple organ dysfunction syndromes (MODS), and deranged glucose homeostasis in mice with sepsis. Aerobic exercise alleviated lung injury partly because aerobic exercise exerted immune effects and activated Sirt-1/Nrf-2 signaling.