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Protective effects of aerobic exercise on acute lung injury induced by LPS in mice

机译:有氧运动对Lps致小鼠急性肺损伤的保护作用

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摘要

Abstract Introduction The regular practice of physical exercise has been associated with beneficial effects on various pulmonary conditions. We investigated the mechanisms involved in the protective effect of exercise in a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods Mice were divided into four groups: Control (CTR), Exercise (Exe), LPS, and Exercise + LPS (Exe + LPS). Exercised mice were trained using low intensity daily exercise for five weeks. LPS and Exe + LPS mice received 200 µg of LPS intratracheally 48 hours after the last physical test. We measured exhaled nitric oxide (eNO); respiratory mechanics; neutrophil density in lung tissue; protein leakage; bronchoalveolar lavage fluid (BALF) cell counts; cytokine levels in BALF, plasma and lung tissue; antioxidant activity in lung tissue; and tissue expression of glucocorticoid receptors (Gre). Results LPS instillation resulted in increased eNO, neutrophils in BALF and tissue, pulmonary resistance and elastance, protein leakage, TNF-alpha in lung tissue, plasma levels of IL-6 and IL-10, and IL-1beta, IL-6 and KC levels in BALF compared to CTR (P ≤0.02). Aerobic exercise resulted in decreases in eNO levels, neutrophil density and TNF-alpha expression in lung tissue, pulmonary resistance and elastance, and increased the levels of IL-6, IL-10, superoxide dismutase (SOD-2) and Gre in lung tissue and IL-1beta in BALF compared to the LPS group (P ≤0.04). Conclusions Aerobic exercise plays important roles in protecting the lungs from the inflammatory effects of LPS-induced ALI. The effects of exercise are mainly mediated by the expression of anti-inflammatory cytokines and antioxidants, suggesting that exercise can modulate the inflammatory-anti-inflammatory and the oxidative-antioxidative balance in the early phase of ALI.
机译:摘要引言经常进行体育锻炼与对各种肺部疾病的有益作用有关。我们在脂多糖(LPS)诱导的急性肺损伤(ALI)模型中研究了运动保护作用涉及的机制。方法将小鼠分为四组:对照组(CTR),运动(Exe),LPS和运动+ LPS(Exe + LPS)。使用低强度的日常运动训练运动的小鼠五周。在最后一次体检后48小时,LPS和Exe + LPS小鼠气管内接受200 µg LPS。我们测量了呼出气一氧化氮(eNO);呼吸力学;肺组织中性粒细胞密度;蛋白质泄漏;支气管肺泡灌洗液(BALF)细胞计数; BALF,血浆和肺组织中的细胞因子水平;肺组织的抗氧化活性;和糖皮质激素受体(Gre)的组织表达。结果LPS滴注导致eNO增加,BALF和组织中的中性粒细胞增加,肺阻力和弹性,蛋白质渗漏,肺组织中的TNF-α,血浆IL-6和IL-10以及IL-1beta,IL-6和KC升高BALF中的水平与CTR相比(P≤0.02)。有氧运动导致肺组织中的eNO水平,中性粒细胞密度和TNF-α表达降低,肺阻力和弹性降低,并导致肺组织中IL-6,IL-10,超氧化物歧化酶(SOD-2)和Gre的水平升高与LPS组相比,BALF中的IL-1beta和IL-1beta差异有统计学意义(P≤0.04)。结论有氧运动在保护肺免受LPS诱导的ALI的炎症作用中起着重要作用。运动的影响主要是由抗炎细胞因子和抗氧化剂的表达介导的,这表明运动可以调节ALI早期的抗炎和抗氧化平衡。

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