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通过观察吸烟小鼠气道上皮细胞凋亡与Myc、Fas表达的动态变化,探讨吸烟致c-myc、fas癌基因活化对小鼠气道上皮细胞凋亡的影响。方法:应用免疫组织化学SABC法和脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)技术,检测不同阶段、不同剂量吸烟时间小鼠气道上皮细胞Myc、Fas表达和细胞凋亡,并进行彩色图像分析。结果:小鼠吸烟4周、12周时,气道上皮细胞Myc和Fas表达及细胞凋亡的面密度与对照组比较明显上调(P<0.01),吸烟剂量加倍时其上调更为明显。吸烟8周时,Myc和Fas表达及细胞凋亡的面密度与对照组之间无显著差异(P>0.05)。结论:吸烟致c-myc、fas癌基因活化诱导气道上皮细胞凋亡可能参与COPD的发生和发展。
The effects of smoking-induced c-myc and fas oncogene activation on the apoptosis of airway epithelial cells in mice were observed by observing the changes of apoptosis and the expression of Myc and Fas in the airway epithelium of smoking mice. Methods: Immunohistochemical SABC method and deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) were used to detect Myc, Fas expression and apoptosis in airway epithelial cells of mice in different stages and different doses of smoking Color image analysis. Results: After being smoked for 4 weeks and 12 weeks, the surface density of Myc and Fas in airway epithelial cells was significantly up-regulated compared with the control group (P <0.01), and the up-regulation was more obvious when the smoking dose was doubled. At 8 weeks after smoking, there was no significant difference in the expression of Myc and Fas between the two groups (P> 0.05). Conclusion: Smoking induced c-myc, fas oncogene activation induced airway epithelial cell apoptosis may be involved in the occurrence and development of COPD.