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目的 观察抗氧化剂—U74 389G对高氧暴露新生大鼠肺内自由基产物、巨噬细胞聚集、硝基酪氨酸形成以及肺细胞增殖活性的影响 ,研究高氧性肺损伤发生机制及各种介质的相互关系 ,探讨抗氧化干预的作用。方法 采用SpragueDawley新生大鼠 95 %O2 暴露 7d建立急性高氧肺损伤模型。应用气相色谱 质谱联用技术测定肺组织羟自由基 ,酶联免疫法测定脂质过氧化产物 8 异前列腺烷 ,免疫组织化学法测定肺内巨噬细胞聚集和硝基化酪氨酸形成 ,3 H TdR掺入法 (放射自显影 )测定肺细胞增殖状况。结果 95 %高浓度氧暴露可致新生大鼠严重肺损伤 ,肺组织羟自由基(2 ,3 DHBA与 2 ,5 DHBA分别为 4 9 2± 3 5 pmol/mg、5 5 8± 2 3pmol/mg)及脂质过氧化产物 (8 异前列腺烷含量为 5 4 6 6± 32 2 pg/mg)与空气对照组比较均显著增加 (P <0 0 5 ) ,肺内巨噬细胞聚集明显 ,蛋白质酪氨酸发生显著硝基化 ,肺上皮细胞增殖停滞。抗氧化剂U74 389G可降低肺组织自由基及其衍生物产生 (2 ,3 DHBA、2 ,5 DHBA与 8 异前列腺烷水平分别为 37 9± 2 4pmol/mg、31 3±1 9pmol/mg和 35 8 5± 2 4 1pg/mg ,P <0 0 5 ) ,减少巨噬细胞聚集和蛋白质硝基化 ,肺上皮细胞增殖部分恢复 ,但未能显著改善高氧所致的肺实质病理?
Objective To investigate the effect of antioxidant-U74 389G on the production of free radical products, macrophage accumulation, nitrotyrosine formation and pulmonary cell proliferation in neonatal rats exposed to hyperoxia, and to investigate the mechanism of hypoxia-induced lung injury The relationship between the media to explore the role of antioxidant intervention. Methods Sprague Dawley rats were exposed to 95% O2 for 7 days to establish acute hyperoxic lung injury model. Hydroxyl radical in lung tissue was determined by gas chromatography-mass spectrometry (GC-MS / MS). Lipoxyperoxide 8-iso-prostanoid was determined by enzyme-linked immunosorbent assay and macrophage aggregation and nitrotyrosine formation in lung were measured by immunohistochemistry. H TdR incorporation (autoradiography) was used to measure the proliferation of lung cells. Results 95% oxygen exposure could cause severe lung injury in neonatal rats. The levels of hydroxyl free radical in lung tissue (2, 3 DHBA and 2, 5 DHBA were 492 ± 35 pmol / mg, 558 ± 23 pmol / mg) and lipid peroxidation products (8 different prostanoids content of 566 ± 32 2 pg / mg) were significantly increased compared with the air control group (P <0 05), macrophage accumulation in the lung significantly, Significant nitration of protein tyrosine, pulmonary epithelial cell proliferation arrest. Antioxidant U74 389G decreased lung tissue free radicals and their derivatives (2, 3 DHBA, 2, 5 DHBA and 8 iso-prostanoids were 37 9 ± 2 4 pmol / mg, 331 ± 1 9 pmol / mg and 35 8 5 ± 2 4 1 pg / mg, P <0 05) to reduce macrophage aggregation and protein nitration, lung epithelial cell proliferation partially restored, but failed to significantly improve the hypoxia-induced pulmonary parenchymal pathology?