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目的 :探讨慢性低氧致气道炎症和肺组织氧化损伤的作用及氨茶碱对其的拮抗作用。方法 :成年雄性Wistar大鼠 34只 ,随机分 3组 :对照组 (n =10 )、低氧组 (n =12 )、氨茶碱干预组 (n =12 )。检测各组大鼠血液及肺组织匀浆中肿瘤坏死因子 -α(TNF -α)、白细胞介素 - 10 (IL - 10 )、脂质过氧化物 (LPO)含量及超氧化物歧化酶(SOD)活性。结果 :与对照组相比 ,低氧组大鼠血液及肺组织匀浆TNF -α、IL - 10、LPO含量显著增高 (P <0 . 0 1) ,SOD活性显著降低 (P <0 .0 1) ,同时 ,肺组织匀浆TNF -α/IL - 10增大 (P <0 .0 1) ;与低氧组相比 ,氨茶碱干预组大鼠血液及肺组织匀浆TNF -α、LPO含量显著降低 (P <0 . 0 1) ,SOD活性、IL - 10水平显著增高 (P <0 .0 1和P <0. 0 5 )。结论 :(1)慢性低氧可引起气道炎症并介导肺组织氧化损伤 ;(2 )氨茶碱具有抗炎和抗氧化作用。
Objective: To investigate the role of chronic hypoxia-induced airway inflammation and lung tissue oxidative damage and the antagonism of aminophylline. Methods: Thirty - four adult male Wistar rats were randomly divided into 3 groups: control group (n = 10), hypoxia group (n = 12) and aminophylline intervention group (n = 12). The levels of tumor necrosis factor - α (TNF - α), interleukin - 10 (IL - 10) and lipid peroxidation (LPO) and the levels of superoxide dismutase SOD activity. Results: Compared with the control group, the content of TNF-α, IL-10 and LPO in the blood and lung tissue of hypoxia group were significantly increased (P <0.01) and the SOD activity was significantly decreased (P <0. 1). At the same time, the level of TNF-α / IL-10 in lung homogenate increased (P <0.01). Compared with hypoxia group, TNF- α in blood and lung homogenate (P <0.01). The activity of SOD and the level of IL - 10 were significantly increased (P <0.01 and P <0.05). Conclusion: (1) Chronic hypoxia can cause airway inflammation and mediate oxidative damage in lung tissue; (2) Aminophylline has anti-inflammatory and anti-oxidative effects.