肺纤维化大鼠血清克拉拉细胞蛋白和表面活性蛋白-D动态变化及早期诊断意义

目的 探讨克拉拉细胞蛋白(CC16)和表面活性蛋白-D(SP-D)在肺纤维化大鼠中的表达水平及早期诊断意义.方法 Wistar大鼠60只随机分为正常对照组(对照组)、博莱霉素致肺纤维化组(模型组).每组30只,分别于造模后1、3、7、14、28 d处死,采用HE、Masson染色观察其肺组织病理变化,碱水解法测定肺组织羟脯氨酸含量,酶联免疫吸附法测定血清CC16、SP-D水平.结果 模型组大鼠肺组织羟脯氨酸含量自第7天[(913.1±69.3)μg/g]起,较对照组[(790.5±36.8)μg/g]升高(P<0.05);血清CC16自第3天[(27.34±0.32)μg/L]开始,低于对照组[(27.85 ±0.32)μg/L](P<0.05),并随病情进展而逐渐降低;血清SP-D各时相均高于对照组(P均<0.05),并且随病情进展而逐渐升高.结论 血清CC16、SP-D在大鼠肺纤维化早期有明显改变,其水平变化可能为肺纤维化的早期诊断提供生物学指标.

Dynamic changes of serum Clara cell protein and surfactant protein-D in rats with pulmonary fibrosis and their value in early diagnosis

Objective To detect the dynamic changes of the level of serum Clara cell protein(CC16)and surfactant protein-D(SP-D)in rats with pulmonary fibrosis induced by bleomycin and to evaluate their value in early diagnosis of pulmonary fibrosis. Methods Sixty Wistar rats were randomly divided into two groups, the control group and bleocin-induced pulmonary fibrotic group,with 30 rats in each group. The rats were killed at 1,3,7,14 and 28 days of treatment Pathology changes of lung tissue were observed by HE,Masson stain,alkaline hydrolysis to assess the hydroxyproline concentration of lung tissue, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of serum CC16 and SP-D. Results The hydroxyproline concentration of lung tissue in the pulmonary fibrotic group ((913. 1 ±69. 3) μg/g) were higher than those of the control group ((790. 5 ± 36. 8) μg/g) from the seventh day(P <0. 05). The levels of serum CC16 of the pulmonary fibrotic group((27. 34 ± 0. 32) μg/L) were lower than those of the control group((27. 85 ±0. 32)μg/L) since the third day(P<0. 05) ,and tended to decrease with the development of the disease. However,the levels of SP-D of the former group were always higher(P <0. 05), and tended to increase with the development of the disease. Conclusions The levels of serum CC16 and SP-D changed considerably in early-stage of pulmonary fibrosis, thus might be used as biomarker for early diagnosis and have some value for pathogenesis of pulmonary fibrosis.