摘要
目的:观察14-3-3蛋白及14-3-3βmRNA在哮喘大鼠肺组织中的表达,探讨布地奈德的抗炎作用机制。方法:利用鸡卵白蛋白(OVA)复制哮喘模型,分别采用免疫组化法和实时荧光定量PCR法检测肺组织14-3-3蛋白及14-3-3βmRNA的表达水平。结果:哮喘组肺组织14-3-3蛋白OD值为0.353±0.023,14-3-3βmRNA OD值为1.78±0.36,显著高于对照组0.211±0.028、1(P<0.01)。布地奈德组14-3-3蛋白OD值为0.310±0.024,显著低于哮喘组(P<0.01);14-3-3βmRNA(1.39±0.51)的表达水平与哮喘组(1.78±0.36)比较差异无统计学意义(P>0.05)。结论:哮喘急性期14-3-3蛋白及14-3-3βmRNA呈现过度表达,可能发挥促炎的作用,但这种表达可以被布地奈德抑制。
Objective: To investigate the possible anti-inflammation roles of budesonide,observe the expressions of 14-3-3 protein and14-3-3β mRNA. Methods: Rats asthma models were challenged by ovalbumin,and the expressions of 14-3-3 protein and 14-3-3βmRNA were determined respectively by immunohistochemisty methods and real-time PCR methods at lung tissue. Results: The expressions of 14-3-3 protein and 14-3-3β mRNA in asthma group( 0. 353± 0. 023 and 1. 78± 0. 36 optical density,respectively) were significantly higher than those in control group( 0. 211 ± 0. 028 and 1 optical density,respectively)( P 0. 01). Noteworthy,the expression of 14-3-3 protein was significantly decreased in budesonide group( 0. 310±0. 024 optical density) than that in asthma group( P 0. 01). Nevertheless,the expressions of 14-3-3β mRNA were not significantly different in budesonide group( 1. 39±0. 51) and asthma group( 1. 78±0. 36)( P 0. 05). Conclusion: The expressions of 14-3-3 protein and 14-3-3β mRNA were overexpressed in asthmatic lung tissue,it may act as a pro-inflammation mediator,but this can be suppressed by budesonide.
出处
《儿科药学杂志》
CAS
2016年第6期5-7,共3页
Journal of Pediatric Pharmacy
基金
温岭市科技局基金资助项目
编号2014-1-59