ICAM-1在实验性肺间质纤维化中的表达及盐酸氨溴索的影响

Expression of ICAM-1 on Pulmonary Interstitial Fibrosis in Rats and the Effect of Ambroxol

目的:观察粘附分子ICAM-1在博来霉素(Blemycine,BLM)所致大鼠肺间质纤维化(Interstitial lungdisease,ILD)过程中的动态变化。探讨盐酸氨溴索(ambroxol,Amb)对大鼠肺ICAM-1及间质纤维化的影响。方法:用博来霉素诱导大鼠肺间质纤维化,观察各组动物肺脏病理组织学改变,肺匀浆丙二醛(MDA)含量变化,通过免疫组织学方法检测各组动物肺脏粘附分子ICAM-1,胶原蛋白Ⅲ(CollagenⅢ)含量。结果:模型组(MOD)大鼠肺组织ICAM-1含量明显增高,盐酸氨溴索(AMB)组大鼠肺组织肺泡炎,肺纤维化程度减轻,ICAM-1,胶原蛋白Ⅲ含量及肺匀浆MDA含量均低于模型组,高于对照组(CON)。结论:ICAM-1是肺间质纤维化进展的重要因子,盐酸氨溴索能抑制ICAM-1在肺组织的表达及肺间胶原蛋白的形成。

Objective： To observe the dynamic change of ICAM-1 of the lung in bleomycin-induced interstitial pulmonary fibrosis in rats and to investigate the effect of ambroxol on ICAM-1 and pulmonary fibrosis. Methods： Forty-five SD rats were divided into three groups in random： control, model and ambroxol-treated group. On experimental day （day 0）, the rats were intratracheally instilled with bleomycin （5 mg · kg^-1 body weight） or sterile saline, and then treated with the ambroxol or saline until they were killed. On day 7, 14, 28 after instillation, five rats of each group were sacrificed and the lungs were harvested for histopathological examination and determination of MDA. The expression of ICAM-1, collagen Ⅲ was measured by means of immunohistochemistry technique. Results： The expression of ICAM-1 in the lungs rose quickly after bleomycin instillatioin and peaked on day 14. The alveolitis and pulmonary fibrosis of ambroxol treated groups were decreased remarkably. The expression level of ICAM-l,collagen Ⅲ of treated group were also decreased than model group. Conclusion： ICAM-1 is a key factor in the development of interstitial pulmonary fibrosis and ambroxol can inhibit the expression of ICAM-1 and pulmonary fibrosis.