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目的观察天然抗氧化剂茶多酚 (Teapolyphenols ,TP)对重复轻度低压缺氧引起的小鼠肺自由基代谢异常的保护作用。方法 42只雄性昆明种小鼠随机分为 3组 :对照组 (A) ;1 50 0m低压缺氧组 (B)和TP保护组 (C)。低压舱暴露时间为 2h/d ,3d/wk ,共 8wk。上舱暴露前 ,C组灌胃给予TP 1 0 0mg/kg ,另 2组给予蒸馏水。末次实验后次日将小鼠断头处死 ,迅速取出肺组织。测定肺超氧化物歧化酶(SOD)活性和丙二醛 (MDA)、一氧化氮 (NO)含量。另外 ,用免疫组化法对肺组织CuZn -SOD和诱生型NO合酶 (iNOS)的含量进行定性观察。结果与对照组比较 ,重复轻度低压缺氧暴露使肺MDA水平和NO含量明显升高 (P <0 .0 1 ) ,但TP防护组肺MDA生成和NO含量恢复正常。B组肺SOD活性有升高趋势 ,该组细支气管上皮细胞CuZn -SOD酶含量和支气管上皮细胞及肺间质血管内皮细胞和平滑肌细胞的iNOS酶含量明显增加。重复给予TP使这些酶的异常表达恢复正常。结论天然抗氧化剂茶多酚对重复轻度低压缺氧引起的肺自由基代谢异常具有保护作用。
Objective To observe the protective effect of natural antioxidants Teapolyphenols (TP) on the metabolism of free radicals in lungs of mice induced by repeated mild hypobaric hypoxia. Methods Forty-two male Kunming mice were randomly divided into three groups: control group (A), hypoxia-hypoxia group (1) at 5050 m and TP protection group (C). Low pressure cabin exposure time 2h / d, 3d / wk, a total of 8wk. Before exposure to the upper chamber, group C was given gavage with TP 100 mg / kg and the other two groups were given distilled water. The mice were decapitated the next day after the last experiment and the lung tissue was quickly removed. The activity of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) and nitric oxide (NO) were measured. In addition, the immunohistochemistry of lung tissue CuZn-SOD and induced NO synthase (iNOS) content qualitative observation. Results Compared with the control group, mild hypobaric hypoxia exposure significantly increased MDA level and NO content in the lung (P <0.01). However, the levels of MDA and NO in lung tissue in TP-treated group were normal. In group B, the activity of SOD in lung increased, the content of CuZn-SOD in bronchial epithelial cells and the content of iNOS in bronchial epithelial cells and pulmonary interstitial vascular endothelial cells and smooth muscle cells increased obviously. Repeated administration of TP restored the abnormal expression of these enzymes. Conclusion The natural antioxidants tea polyphenols have a protective effect on abnormal metabolism of free radical in the lungs induced by repeated hypobaric hypoxia.