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目的探讨安可临对二氧化硅(SiO2)粉尘所致大鼠肺氧化损伤的保护作用。方法将30只雄性大鼠(体质量约为200g)随机分为阴性对照组、矽肺模型组和安可临治疗组(简称“治疗组”),每组10只。采用非暴露式气管内注入法染尘,矽肺模型组和治疗组每只大鼠注入1ml 50mg/ml SiO2混悬液,治疗组于染尘第2天开始每天灌胃给予Oncolyn进行干预。饲养28d后测定大鼠肺泡巨噬细胞凋亡率,肺泡灌洗液(BALF)和肺组织中的总蛋白含量、总抗氧化能力(T-AOC)、丙二醛(MDA)含量、羟脯氨酸(HYP)含量;观察肺脏病理形态学改变。结果治疗组肺巨噬细胞凋亡率高于对照组但低于模型组;BALF和肺组织匀浆中,模型组和治疗组MDA含量和HYP含量均高于阴性对照组,而T-AOC含量低于对照组,且模型组HYP含量高于治疗组,T-AOC含量低于治疗组(P<0.05);BALF中模型组和治疗组MDA含量比较,差异无统计学意义(P>0.05);而在肺组织匀浆中MDA含量模型组高于治疗组(P<0.05);病理形态学显示,治疗组比模型组肺脏纤维化程度较轻。结论安可临对于SiO2粉尘所致肺氧化损伤有一定的保护作用。
Objective To investigate the protective effect of Andacolin against oxidative damage of lung in rats induced by silica (SiO2) dust. Methods Thirty male rats (weighing about 200 g) were randomly divided into negative control group, silicosis model group and Amoxicillin treatment group (referred to as “treatment group”), with 10 in each group. In the non-exposed endotracheal intratracheal instillation method, 1ml 50mg / ml SiO2 suspension was injected into each group of the silicosis model group and the treatment group. The treatment group was orally administered Oncolyn intragastrically on the 2nd day after the dying. After 28 days of feeding, the apoptosis rate of alveolar macrophages, the total protein content in BALF and lung tissue, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, The contents of HYP in the lungs were observed. Pathological changes of the lungs were observed. Results The apoptosis rate of lung macrophages in treatment group was higher than that in control group but lower than that in model group. In BALF and lung homogenate, MDA content and HYP content in model group and treatment group were higher than those in negative control group, while T-AOC content (P <0.05). Compared with the control group, the content of HYP in the model group was higher than that in the treatment group and the content of T-AOC in the model group was lower than that in the treatment group (P <0.05). There was no significant difference in MDA content between the model group and the treatment group ; While in the lung tissue homogenate, the content of MDA in the model group was higher than that in the treatment group (P <0.05). The histopathology showed that the lung fibrosis was lighter in the treatment group than in the model group. Conclusions Arocloxin can protect the lung against oxidative damage induced by SiO2 dust.