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目的探讨铀矿尘致大鼠肺纤维化过程中,肺组织和血浆中转化生长因子-β1(TGF-β1)、一氧化氮(NO)水平变化。方法 60只成年Wistar大鼠,随机分为铀矿尘组与对照组。采用一次性非暴露式气管灌注法,铀矿尘组一次性气管内灌注质量浓度为20 g/L铀矿粉尘悬液1 ml,对照组一次性气管内灌注生理氯化钠溶液1 ml。每组分别于染尘后第7、14、21、30及60天随机处死6只动物,取周围血及肺组织。肺组织形态学观察采用HE染色法;肺组织及血浆中TGF-β1水平的测定采用酶联免疫吸附法(ELISA法);肺组织及血浆中NO水平的测定采用硝酸还原酶法。结果实验观察期内铀矿尘致大鼠肺组织纤维增生病变;铀矿尘在致肺组织纤维化过程中,可引起肺组织及血浆中TGF-β1及NO水平增高,且在染尘后第30、60天时其肺组织和血浆中TGF-β1及NO水平与对照组比较,差异有统计学意义(P<0.05);肺组织与血浆中TGF-β1及NO水平变化存在直线正相关(rTGF=0.887,P<0.05;rNO=0.958,P<0.05)。结论在铀矿尘致大鼠肺纤维化过程中,其肺组织和血浆中TGF-β1和NO的水平可见明显增高,肺组织与血浆中TGF-β1及NO水平变化存在直线正相关。
Objective To investigate the changes of the levels of transforming growth factor-β1 (TGF-β1) and nitric oxide (NO) in lung tissue and plasma during pulmonary fibrosis induced by uranium dust in rats. Methods Sixty adult Wistar rats were randomly divided into uranium dust group and control group. A one-time non-exposed tracheal perfusion method was used. One-time endotracheal perfusion of uranium dust group was 1 ml of uranium dust suspension with a mass concentration of 20 g / L, and a control group was infused with 1 ml of physiological sodium chloride solution. Six animals were randomly sacrificed on the 7th, 14th, 21st, 30th and 60th days after the dying respectively. Peripheral blood and lung tissues were collected. The morphology of lung was observed by HE staining. The level of TGF-β1 in lung tissue and plasma was determined by enzyme-linked immunosorbent assay (ELISA). Nitric acid reductase was used to determine the level of NO in lung tissue and plasma. Results During the observation period, the uranium mine dust caused lung fibrosis in rats. Uranium dust induced lung fibrosis and TGF-β1 and NO levels in lung tissue and plasma. The levels of TGF-β1 and NO in lung tissue and plasma at 30 and 60 days were significantly different from those in control group (P <0.05). There was a positive correlation between the levels of TGF-β1 and NO in lung tissue (rTGF = 0.887, P <0.05; rNO = 0.958, P <0.05). Conclusion The levels of TGF-β1 and NO in lung tissue and plasma of rats with uranium dust-induced lung fibrosis were significantly increased. There was a linear positive correlation between the levels of TGF-β1 and NO in lung tissue.