摘要
目的研究与肥大细胞功能相关的microRNA在卵清蛋白(OVA)诱导的支气管哮喘小鼠模型中的表达差异。方法采用OVA诱导的支气管哮喘小鼠模型,通过检测肺泡灌洗液(BALF)中细胞数及组织病理验证模型的成功建立。应用实时荧光-PCR法检测支气管哮喘小鼠模型肺组织microRNA-223、microRNA-221、microRNA-15、microRNA-374、microRNA-27与正常对照组的表达差异。结果 OVA诱导的支气管哮喘小鼠模型组BALF中细胞总数(12.8±2.2)较正常对照组(5.6±2.5)显著升高(P<0.05);嗜酸性粒细胞数(6.6±1.9)较正常对照组(0.8±0.8)显著升高(P<0.05)。组织病理显示支气管哮喘模型组大鼠炎症细胞浸润明显高于正常对照组。在支气管哮喘组大鼠,microRNA-223的表达约为正常对照组大鼠的3倍(P<0.05);microRNA-532的表达约为正常对照组大鼠的0.5(P<0.05);microRNA-15的表达约为正常对照大鼠的0.4(P<0.05);microRNA-221的表达约为正常对照大鼠的2.5(P<0.05);microRNA-27的表达约为正常对照大鼠的0.2(P<0.05)。结论 5条与肥大细胞功能相关的microRNA在OVA诱导的支气管哮喘小鼠模型中存在差异表达,差异表达的microRNA可能通过调节肥大细胞的功能,参与支气管哮喘的发病。
Objective To investigate the different expressions of microRNA in murine asthma model induced by ovalbumin(OVA). Methods OVA-induced murine asthma model was used in this study.The cell number in bronchoalveolar lavage fluid(BALF) of murine asthma model and lung histological study was assed.Expression of microRNA(microRNA-223,microRNA-221,microRNA-15,microRNA-374,microRNA-27)in ova-induced asthma in a mouse model was analyzed by real time-PCR. Results The cell number was significantly higher in BALF of murine asthma model group(12.8±2.2) than that of normal control group(5.6±2.5)(P〈0.05).Enhanced eosinophilic inflammation in lung was observed in murine asthma model group(6.6±1.9) compared with the normal controls(0.8±0.8)(P〈0.05). The infiltration of leukocytes to lung tissue was upregulated in OVA-induced murine asthma model compared to the controls. Compared to the controls,microRNA-223(about 3 fold,P〈0.05),microRNA-221(about 2.5 fold,P〈0.05) were upregultaed.MicroRNA-532(about 0.5 fold,P〈0.05),microRNA-15(about 0.4 fold,P〈0.05),microRNA-27(about 0.2 fold,P〈0.05) were downregulated. Conclusion These mast cell function related microRNA have differential expressions in murine asthma model induced by OVA,and the microRNA may take part in murine asthma through regulating the function of mast cell.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2012年第21期1655-1657,共3页
Journal of Applied Clinical Pediatrics
基金
南京市医学科技发展资金资助项目(QYK09163)