文章摘要
崔晶,王晨宇,王聪聪,等.有氧运动训练改善2型糖尿病大鼠肺损伤的疗效观察[J].中华物理医学与康复杂志,2026,48(6):494-500
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有氧运动训练改善2型糖尿病大鼠肺损伤的疗效观察
  
DOI:10.3760/cma.j.cn421666-20251023-00949
中文关键词: 有氧运动  糖尿病  肺功能  糖尿病性肺病  氧化还原平衡
英文关键词: Aerobic exercise  Diabetes mellitus  Lung function  Diabetic pneumopathy  Redox status
基金项目:
作者单位
崔晶 郑州工商学院体育学院,郑州 451400 
王晨宇 郑州航空工业管理学院,郑州 450046 
王聪聪 武警后勤学院卫生勤务系,天津 300309 
杨进华 郑州大学第一附属医院心内科,郑州 450001 
牛晓阳 郑州大学第五附属医院康复科,郑州 450001 
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中文摘要:
      目的 探讨中等强度有氧运动对2型糖尿病大鼠模型肺损伤的改善作用,为糖尿病性肺病防治提供参考资料。 方法 采用随机数字表法将45只Wistar大鼠分为对照组、模型组和运动组,每组15只。通过向腹腔注射链脲佐菌素(STZ)方式将模型组及运动组大鼠制成2型糖尿病模型。运动组大鼠在造模4周后给予12周中等强度跑台训练,对照组及模型组大鼠则同期置于鼠笼内安静饲养。于训练前、后检查各组大鼠血糖、体质量及摄食量改变,并进行口服葡萄糖耐量试验(OGTT),采用递增负荷跑台实验评估大鼠运动功能,采用强迫振荡技术检测大鼠肺功能,采用苏木精-伊红(HE)染色观察大鼠肺组织病理学改变,采用分光光度法测定大鼠肺脏丙二醛(MDA)含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性。 结果 与对照组比较,模型组大鼠空腹及餐后血糖显著升高(P<0.05),葡萄糖耐量受损(P<0.05),体质量减轻(P<0.05),摄食量增加(P<0.05),肺力学参数如牛顿阻力、粘性、弹性及滞后率均显著增加(P<0.05),肺组织结构紊乱(如肺泡塌陷、肺动脉壁和肺间隔增厚、炎性细胞浸润等),MDA含量明显升高(P<0.05),SOD及CAT活性均显著下降(P<0.05),运动功能下降(P<0.05)。与模型组比较,运动组大鼠空腹及餐后血糖明显下降(P<0.05),葡萄糖耐量增强(P<0.05),摄食量减少(P<0.05),肺机械功能及肺组织病理损伤改善(P<0.05),MDA含量降低(P<0.05),SOD及CAT活性均显著升高(P<0.05),运动能力明显增强(P<0.05)。 结论 中等强度有氧运动可有效改善2型糖尿病大鼠模型肺损伤,其作用机制可能与降低氧化应激水平、恢复抗氧化酶活性有关。
英文摘要:
      Objective To document any ameliorative effect of moderate-intensity aerobic exercise when a lung injury is complicated by type 2 diabetes mellitus. Methods Forty-five Wistar rats were randomly divided into a control group, a model group, and an exercise group, each of 15. Type 2 diabetes mellitus was induced in the model and exercise groups by intraperitoneal injection of streptozotocin. Four weeks later, the exercise group began 12 weeks of moderate-intensity treadmill training, while the other two groups were housed quietly in their cages. Before and after the training, changes in blood glucose, body mass, and food intake were measured, and an oral glucose tolerance test was performed. Exercise capacity was evaluated using an incremental load treadmill test, and a forced oscillation technique evaluated lung functioning. Any histopathological changes in lung tissue were observed using hematoxylin-eosin staining. Levels of pulmonary malondialdehyde (MDA) and superoxide dismutase (SOD), and catalase (CAT) activity were determined by spectrophotometry. Results Compared with the control group, the model group showed a significant increase in fasting and postprandial blood glucose, on average, and in average food intake, MDA content, and in Newtonian resistance, tissue viscance, elastance and hysteresis in the lungs. But there had been a significant decrease in SOD and in CAT activity, body mass and exercise capacity, together with impaired glucose tolerance, and disordered lung tissue structure (e.g., alveolar collapse, thickening of pulmonary artery walls and alveolar septa, inflammatory cell infiltration). Comparing the exercise group with the model group, there was significantly decreased fasting and postprandial blood glucose, food intake and MDA content, but enhanced glucose tolerance, improved pulmonary mechanics and histopathology. There was also significantly increased SOD and CAT activity, on average, and greater exercise capacity. Conclusions Moderate-intensity aerobic exercise can effectively ameliorate lung injury in the presence of type 2 diabetes, at least in rats. The mechanism involved may be associated with reducing oxidative stress and restoring antioxidant enzyme activities.
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