过氯酸铵对大鼠肺组织Ⅰ型和Ⅲ型胶原mRNA表达的研究

Expressions of collagen in lung of rats exposed to ammonium perchlorate

目的探讨过氯酸铵（AP）对大鼠肺组织Ⅰ型和Ⅲ型胶原表达的影响。方法大鼠气管内一次性注入AP染毒，AP染毒剂量分低、中、高3个剂量组（48、96、192mg／kg），同时设阴性对照组（生理盐水）和阳性对照组（博来霉素5mg／kg）。分别于第3、7、14、28天处死大鼠。通过逆转录聚合酶链式反应（RT-PCR）测定Ⅰ型、Ⅲ型胶原mRNA表达水平。结果高剂量组第7、14、28天（1．93±0．41、3．50±0．90、2．33±1．12）以及中剂量组第28天（2．58±0．86）Ⅰ型胶原mRNA表达水平分别明显高于阴性对照组，差异有统计学意义（P〈0．05）；低剂量组第14、28天和高剂量组第14天Ⅰ型胶原mRNA表达水平（1．99±0．67、1．85±0．67、3．50±0．90）比同组第3天明显升高，差异有统计学意义（P〈0．05）。第14、28天中剂量组（1．80±0．51、2．16±0．87）和高剂量组（2．60±1．00、1．46±0．36）m型胶原mRNA表达水平比阴性对照组明显升高，差异有统计学意义（P〈0．05或P〈0．01）；高剂量组第14天（2．60±1．00）和中剂量组第28天（2．16±0．87）Ⅲ型胶原mRNA表达比第3天明显升高，差异有统计学意义（P〈0．05）。结论AP可使大鼠肺组织Ⅰ型、Ⅲ型胶原mRNA表达明显升高，但AP是否具有致肺纤维化作用，仍需进一步深入研究。

Objective To study the influence on expression of interstitial collagen in lung of rats exposed to ammonium perchlorate. Methods The rats were treated with AP by intratracheal instillation and sacrificed after 3 d, 7 d, 14 d, 28 d. The mRNA level of collagen Ⅰ and collagen Ⅲ in the lung tissues was measured by RT-PCR. Results The levels of collagen Ⅰ on 7 d, 14 d, 28 d exposed for high dose group （ 1.93 ± 0.41,3.50±0.90,2.33±1.12） and 28d exposed for medial dose group（2.58±0.86）were higher significantly （P〈 0.05） than those in negative control group （0.52±0.11,0.77±0.15,0.86±0.29）; The levels of collagen Ⅰ in low dose group exposed for 14 d（1.99±0.67）, 28 d（1.85±0.67） and high dose group 14 d（3.50±0.90） exposed for 14 d were higher significantly （P〈0.05） compared to those exposed to AP for 3 d（0.52±0.14,1.71±0.38）. The levels of collagen Ⅲ on 14 d, 28 d exposed for high dose group（2.60±1.00,1.46±0.36） and 14 d, 28 d exposed for medial dose group （1.80±0.51,2.16±0.87） were higher significantly （P〈0.05 or P〈0.01） than those in negative control group（0.54±0.20,0.52±0.22） ; The levels of collagen Ⅲ in medial dose group（2.16±0.87） exposed for 28 d, and high dose group exposed for 14 d （2.60±1.00） were higher significantly（P〈0.05） compared to those exposed to AP for 3 d（1.22±0.32,0.96±0.17）. Conclusion The results suggest that AP has a toxic effect to promote the expressions of collagen Ⅰ and collagen Ⅲ mRNA in lungs of rats, and may cause fibrosis, but there should have more sufficient evidences to prove that AP is exactly the compound that causes lung fibrosis.