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在制备人和小鼠的Ｐｒｏαｌ（Ⅰ）、Ｐｒｏαｌ（Ⅲ）前胶原ｃＤＮＡ探针的基础上，采用ｃＤＮＡ－ｍＲＮＡ斑点杂交及原位杂交技术，观察了二氧化硅诱导二个月和四个月的矽肺纤维化大鼠肺组织Ⅰ型、Ⅲ型胶原基因的ｍＲＮＡ水平和分布情况。实验结果表明，肺纤维化组织中Ｐｒｏαｌ（Ⅰ）、Ｐｒｏαｌ（Ⅲ）ｍＲＮＡ含量比正常肺组织明显增加（Ｐ＜０．０５），两型ｍＲＮＡ在正常肺组织主要分布于肺泡间隔的成纤维细胞中，而在病变组织主要分布于细胞性结节和增厚间质的成纤维细胞中。我们认为二氧化硅诱导的矽肺纤维出组织中胶原纤维的增生和积聚与胶原基因的表达密切相关。
Based on the cDNA probes of Proαl (Ⅰ) and Proαl (Ⅲ) procollagen in human and mouse, cDNA-mRNA dot blot hybridization and in situ hybridization were used to observe the effects of silica-induced two months and four months Of lung fibrosis rats with type Ⅰ, type Ⅲ collagen gene mRNA levels and distribution. The results showed that the contents of Proαl (Ⅰ) and Proαl (Ⅲ) mRNA in lung fibrosis tissues were significantly higher than those in normal lung tissues (P <0.05). The two types of mRNA in normal lung tissues were mainly distributed in alveolar septa fibroblasts , While in diseased tissues are mainly distributed in the cell nodules and thickened interstitial fibroblasts. We think that collagen-induced hyperplasia and accumulation of collagen fibers in the silica-induced fibrosis tissue are closely related to collagen gene expression.