论文部分内容阅读
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 observe the expression of 14-3-3 protein and 14-3-3βmRNA in the lung tissue of asthmatic rats and explore the anti-inflammatory mechanism of budesonide. Methods: Asthmatic model was established by using ovalbumin (OVA). The expressions of 14-3-3 protein and 14-3-3β mRNA in lung tissue were detected by immunohistochemistry and real-time fluorescence quantitative PCR respectively. Results: The OD value of 14-3-3 protein in lung tissue of asthma group was 0.353 ± 0.023, and the OD value of 14-3-3β mRNA was 1.78 ± 0.36, which was significantly higher than that of control group (0.211 ± 0.028,1, P <0.01). The OD value of 14-3-3 protein in budesonide group was 0.310 ± 0.024, which was significantly lower than that in asthma group (P <0.01). Compared with asthma group (1.78 ± 0.36), the expression level of 14-3-3β mRNA (1.39 ± 0.51) The difference was not statistically significant (P> 0.05). CONCLUSION: The 14-3-3 protein and 14-3-3βmRNA are overexpressed in the acute phase of asthma and may play a proinflammatory role, but this expression may be inhibited by budesonide.