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目的:探讨细胞凋亡在爆炸致兔急性肺损伤(ALI)中的作用机制。方法:选取兔40只,随机分为空白对照组10只;实验组30只,空气爆炸损伤胸部,制作ALI模型,分别于爆炸损伤4、12、24 h后采样(每时间点各10只),测定肺干/湿重比、动脉血氧分压,原位末端标记检测肺组织细胞凋亡情况,免疫组织化学法检测Caspase-3、Bax、Bcl-2含量。选取肺组织,显微镜观察光镜下肺组织病理形态。结果:光镜下,实验组4 h起可见肺间质、肺泡明显水肿,肺泡腔大量红细胞、炎性细胞及浆液性渗出,肺间质增厚。与对照组比较,各实验组肺干/湿重比均明显升高(P<0.01),动脉血氧分压均明显降低(P<0.01)。凋亡指数均明显升高(P<0.01),Caspase-3与Bax/Bcl-2比值均较对照组升高(P<0.05~P<0.01)。结论:细胞凋亡在兔ALI的发生、发展过程中起重要作用,参与了肺组织损伤,促进ALI病情进展。
Objective: To investigate the mechanism of apoptosis in the acute lung injury caused by explosion in rabbits (ALI). Methods: Forty rabbits were randomly divided into blank control group (n = 10), experimental group (n = 30) and air burst injury to the thorax. ALI models were made and samples were taken at 4,12,24 h after explosion injury (10 at each time point) The lung dry / wet ratio, arterial partial pressure of oxygen and the apoptosis of lung tissue were detected by in situ end-labeling. The contents of Caspase-3, Bax and Bcl-2 were detected by immunohistochemistry. Pulmonary tissue was selected and the pathological changes of lung tissue under light microscope were observed. Results: Under the light microscope, the experimental group 4 h showed pulmonary interstitial, significant alveolar edema, alveolar a large number of red blood cells, inflammatory cells and serous exudation, pulmonary interstitial thickening. Compared with the control group, the lung dry weight / wet weight ratio in each experimental group were significantly increased (P <0.01), and the arterial oxygen partial pressure was significantly decreased (P <0.01). (P <0.01). The ratio of Caspase-3 to Bax / Bcl-2 was higher than that of the control group (P <0.05 ~ P <0.01). Conclusion: Apoptosis plays an important role in the occurrence and development of ALI in rabbits, which is involved in the lung injury and promoting the progression of ALI.