高氧所致慢性肺损伤早产鼠肺纤维化与p16蛋白的变化  

Pulmonary fibrosis and expression of p16 protein in premature rats with hyperoxia-induced chronic lung disease

作　　者：麦友刚[1] 吴燕云[1] 赖文玉[1] 林素暇[2] 张红珊[1] 苏浩彬[1] 

机构地区：[1]中山大学附属第二医院儿科,广州510120 [2]中山大学肿瘤防治中心病理科,广州510060

出　　处：《广东医学》2010年第17期2225-2227,共3页Guangdong Medical Journal

基　　金：广东省自然科学基金资助项目(编号:7001588)

摘　　要：目的观察高氧所致慢性肺损伤早产鼠的肺纤维化与p16蛋白的变化情况。方法将120只早产鼠随机分为对照组、高氧CLD组和地塞米松组,每组40只,采用高浓度氧诱导CLD模型,于实验第1、3、71、4、21天分别应用酶联免疫吸附法及免疫组织化学技术检测其肺组织Ⅰ型胶原和p16蛋白表达。结果与对照组比较,高氧CLD组第14天和第21天肺纤维化评分及Ⅰ型胶原水平增加,p16蛋白表达水平降低;产前地塞米松治疗可减轻高氧暴露后早产鼠肺纤维化评分及Ⅰ型胶原水平,但对p16蛋白表达水平降低无影响。结论高氧诱导早产鼠肺组织p16蛋白表达水平降低,可能与CLD肺纤维化的发生机制有关系。Objective To observe the dynamic change in the expression of p16 protein and pulmonary fibrosis in premature rats with hyperoxia-induced chronic lung disease（CLD）. Methods One hundred and twenty premature rats were random1y divided into control group（room air group）,hyperoxia group（CLD group） and antenatal dexamethsone treatment group.CLD was induced by hyperoxia exposure.The levels of type I collagen and p16 were measured with enzyme linked immunosorbent assay and immunohistochemical method,respectively,on day 1,3,7,14 and 21. Results Compared with those in the control group,the scores of interstitial fibrosis in lung and the level of type I collagen significantly increased,while the expression of p16 protein was reduced on day 14 and 21 in CLD group.Compared with those in CLD group,though the scores of interstitial fibrosis in lung and the level of type I collagen were significantly reduced,no significant difference in the expression of p16 protein was observed in antenatal dexamethsone treatment group. Conclusion Hyperoxia exposure reduces the expression of p16 protein in premature rats,leading to lung fibrosis.

关 键 词：高氧 早产 鼠 P16蛋白 肺纤维化 

分 类 号：R735.202[医药卫生—肿瘤]