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[目的 ]探讨过氯酸铵 (AP)致动物肺纤维化作用。 [方法 ]①小鼠胚胎肺成纤维细胞染毒AP 48h后测定羟脯氨酸 (HYP)含量 ;②大鼠经气管内注入AP染毒 7～ 2 9d ,取大鼠肺泡灌洗液 (BALF)和肺组织 ,测定肿瘤坏死因子 α(TNF α)、丙二醛 (MDA)、HYP和胶原蛋白 (Collagen)的含量 ,并对肺组织进行病理检查。 [结果 ]①病理结果显示AP能引起肺急性炎症反应 ,但没有明显的肺纤维化病变 ;②AP染毒小鼠胚胎肺成纤维细胞HYP含量变化不显著 ;③AP低剂量组TNF α含量显著高于阴性对照组 (P <0 .0 1) ,尤其是低剂量第 2 9d组 ;④AP染毒后第 7d高剂量组MDA、HYP、Collagen含量明显高于阴性对照组 (P <0 .0 1) ,呈接触剂量 效应关系。 [结论 ]AP能引起肺急性炎症反应 ,对TNF α、MDA、HYP和collagen合成有一定影响 ;本实验尚不能证明AP有致肺纤维化作用
[Objective] To investigate the pulmonary fibrosis induced by ammonium perchlorate (AP). [Method] ① The content of hydroxyproline (HYP) in mouse embryonic lung fibroblasts after 48h exposure to AP was measured. ② The rats were subjected to endotracheal injection of AP for 7 ~ 29 days. BALF ) And lung tissue. The content of tumor necrosis factor alpha (TNFα), malondialdehyde (MDA), HYP and Collagen were measured, and lung tissue was examined by pathology. [Results] ① The pathological results showed that AP could cause acute pulmonary inflammatory response, but no obvious pathological changes of pulmonary fibrosis. ② The content of HYP in APF-treated mouse embryo lung fibroblasts did not change significantly. ③ The content of TNFα in AP low-dose group was significantly higher than that of AP (P <0.01), especially in the low dose group (29d). ④ The levels of MDA, HYP and Collagen in the high dose group at 7th day after AP were significantly higher than those in the negative control group (P <0.01) , Was exposed to dose-effect relationship. [Conclusion] AP can cause acute inflammatory reaction of lung, which has certain influence on the synthesis of TNFα, MDA, HYP and collagen; this experiment can not prove that AP has pulmonary fibrosis