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目的 探讨Bax和Bcl- 2表达的变化在ARDS发病中的作用 ,试图为进一步阐明ARDS的发病机制和在细胞凋亡水平防治本病提供理论依据。方法 ARDS组 9例 ,对照组 5例 ,采用TUNEL法以及免疫组化技术观察ARDS患者肺组织细胞凋亡及Bax和Bcl- 2表达的变化。结果 ARDS急性期患者肺组织细胞凋亡率较对照组明显增加 ,且主要表现为肺泡上皮和肺血管内皮细胞凋亡增加 ;Bcl- 2表达ARDS组和对照组无显著差异 ,Bax在ARDS急性期患者肺组织表达明显上调 ,并且Bax表达的增加与肺组织细胞凋亡增加呈平行关系。结论 肺泡上皮和肺血管内皮细胞凋亡改变和Bax/Bcl- 2表达的变化可能参与临床ARDS急性期的发病。
Objective To investigate the role of Bax and Bcl-2 expression in the pathogenesis of ARDS and to provide a theoretical basis for further elucidating the pathogenesis of ARDS and preventing and treating this disease at the level of apoptosis. Methods Nine patients in ARDS group and five in control group were used to observe the changes of apoptosis and expression of Bax and Bcl-2 in lung tissue of ARDS patients by TUNEL method and immunohistochemistry. Results The apoptotic rate of lung tissue in patients with ARDS was significantly higher than that of the control group, and the apoptotic rate was significantly higher in alveolar epithelial cells and pulmonary vascular endothelial cells. There was no significant difference in the expression of Bcl-2 between ARDS group and control group. The lung tissue of patients was significantly up-regulated, and the increase of Bax expression was in parallel with the increase of lung cell apoptosis. Conclusion The changes of apoptosis of alveolar epithelial cells and pulmonary vascular endothelial cells and the changes of Bax / Bcl-2 expression may be involved in the pathogenesis of acute ARDS.