摘要
目的 :观察急性肺损伤 (ALI)时小鼠肺组织损伤程度与角质细胞生长因子受体 (KGFR)表达水平的关系 ,为基因治疗急性肺损伤提供依据。方法 :建立脂多糖 (LPS)造成的小鼠肺损伤模型和Ⅱ型肺泡上皮细胞 (A5 49细胞 )损伤模型 ,通过病理分析、反转录聚合酶链反应 (RT PCR)和荧光定量聚合酶链反应 (FQ PCR)观察肺组织损伤程度与KGFR表达水平的关系。结果 :LPS造成轻度、中度和重度肺损伤时肺组织KGFR表达水平逐步下降 ,各种损伤程度之间KGFR表达存在显著差异 (P <0 .0 5 )。A5 49细胞的KGFR表达变化不明显 (P >0 .0 5 )。结论 :随着肺损伤程度的加重 ,肺组织KGFR表达水平逐次减低 。
Objective: To explore evidence of acute lung injury (ALI) gene therapy with analysing relations between the degrees of mouse lung injury and expressions of KGFR.Method: The injured models of mouse lung and alveolar type Ⅱ(A549) were established by lipopolysaccharide(LPS). Relations between the degrees of mouse lung injury and expressions of KGFR were observed by using pathological analysis and reverse transcription-polymerase chain reaction(RT-PCR), fluorescent quantitative-polymerase chain reaction(FQ-PCR).Results: The mouse lung injured by LPS as longitudinal,medial and serious degree.The KGFR expressions of lung gradually decreased, there are significant difference among all degrees of lung injury(P<0.05).But the KGFR expressions of A549 isn't significant difference(P>0.05).Conclusion: The more serious degree of lung injury, the more decrease of KGFR expression is. ALI do great damage to KGFR expression.
出处
《微循环学杂志》
2004年第2期18-20,F004,共4页
Chinese Journal of Microcirculation
基金
20 0 2年国家自然科学基金资助项目 (No.3 0 2 713 43 )
关键词
脂多糖
小鼠
急性肺损伤
组织病理
角质细胞
生长因子
受体表达
ALI
肺组织
Acute lung injury(ALI)
Keratinocyte growth factor receptor (KGFR)
Lipopolysaccharide(LPS)
Reverse transcription-polymerase chain reaction(RT-PCR)
Fluorescent quantitative-polymerase chain reaction(FQ-PCR)
