【摘要】 目的 :探讨肺气虚证细胞凋亡机制。方法 :用两次气管内注入脂多糖 (LPS)及熏香烟 4周的复合刺激法复制肺气虚证大鼠模型 ,4周后对两组动物进行电镜观察和免疫组化检测。结果 :与对照组比较 ,模型组可见肺组织细胞凋亡明显增加 ,Fas、FasL蛋白在肺组织中的表达明显上调。结论 :Fas、FasL可能参与了肺气虚的发病及肺组织细胞凋亡的调控。更多还原

【Abstract】 Objective:To evaluate the expression of apoptosis related genes in rats with pulmonary Qi deficiency. Method: The rat pulmonary Qi deficiency model was established by intratracheal instillation of lipopolysaccharide(LPS) twice and exposed to cigarette smoke. By transmission electron microscope (TEM) and immunocytochemistry techniques, apoptosis and Fas,FasL protein expression were studied in two groups after 4 weeks. Result: Apoptosis ratio was obviously higher in the model group than that in the control group. Fas and FasL protein expression of lung tissues were up regulated in the model group.Conclusion:Fas and FasL may contribute to the pathogenesis of pulmonary Qi deficiency,and participate in cell apoptosis modulation of the lung tissues with pulmonary Qi deficiency.更多还原