| 摘要: |
| 目的：观察14-3-3蛋白及mRNA在哮喘大鼠肺组织中表达，探讨布地奈德的抗炎作用机制。方法：利用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mRNA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及14-3-3β mRNA为1.78±0.36，显著高于对照组（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）；14-3-3β mRNA（1.39±0.51）的表达水平与哮喘组比较差异无统计学意义（P>0.05）。结论：哮喘急性期14-3-3呈现过度表达，可能起了促炎的作用，但这种表达可以被布地奈德所抑制。 |
| 关键词: 哮喘 14-3-3蛋白 糖皮质激素 发病机制 |
| DOI：doi:10.13407/j.cnki.jpp.1672-108X.2016.06.002 |
|
| 基金项目:温岭市科技局基金资助项目，编号2014-1-59。 |
|
| Roles of Budesonide on 14-3-3 Protein and mRNA Expression at Asthmatic Rat Lung Tissue |
| He Shujuan1, Chen Ya1, Tong Xiasheng2, Yan Wenhui3, Jiang Zhenfeng4 |
| (1. Enze Women & Children’s Hospital Affiliated to Zhejiang Enze Medical Group, Zhejiang Taizhou 317500, China; 2. Taizhou Integrated Western and Traditional Chinese Medicine Hospital, Zhejiang Taizhou 317500, China; 3. Wenling Traditional Chinese Medical Hospital, Zhejiang Taizhou 317500, China; 4. Wenling Health Education School, Zhejiang Taizhou 317500, China) |
| Abstract: |
| Objective: To investigate the possible anti-inflammation roles of budesonide, the expression of 14-3-3 protein was observed in asthmatic rat lung tissue. Methods: Rats asthma model were challenged by ovalbumin, and the expressions of 14-3-3 protein and mRNA was determined respectively by immunohistochemisty methods or Real-time PCR methods at lung tissue. Results: The expressions of 14-3-3 protein and mRNA in asthma group (0.353±0.023 optical density; 1.78±0.36, respectively) were significantly higher than those in control group (0.211±0.028 optical density; 1, respectively; all P<0.01). Noteworthy, the expressions of 14-3-3 protein were 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 was not statistically significant difference in between budesonide group (1.39±0.51) and asthma group (P>0.05). Conclusion: The 14-3-3 protein were overexpressed in asthmatic lung tissue, it may act as a pro-inflammation mediator, but this function of 14-3-3 protein can be suppressed by budesonide. |
| Key words: asthma 14-3-3 protein glucocorticoid pathogenesis |
