爆炸致兔急性肺损伤时细胞凋亡作用机制的研究

    The mechanism of cell apoptosis in rabbit with acute lung injury induced by blast

    • 摘要: 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。

       

      Abstract: Objective: To investigate the mechanism of cells apoptosis in rabbit with acute lung injury(ALI) induced by blast. Methods: Forty rabbits were randomly divided into the control group(n=10) and experimental group(n=30). The ALI model of rabbit was established by air blast. After 4, 12 and 24 hours of lung injury, the cells apoptosis of injury tissue were detected using the wet/dry weight ratio(W/D) of lung, PaO2 and TUNEL, the levels of caspase-3, Bax and Bcl-2 were detected using immunohistochemistry and the pathological morphology were observed under microscopy in 10 rabbits each time-point. Results: The pulmonary interstitial and alveolar edema, a large number of red blood cells, inflammatory cells and serous effusion in alveolar space, and pulmonary interstitial thickening were found in experimental group under light microscope. Compared with the control group, the W/D and PaO2 in experimental group increased and decreased significantly, respectively(P<0.01), The apoptosis index, caspase-3 and Bax/Bcl-2 in experimental group were significantly higher than those in control group(P<0.05 to P<0.01). Conclusions: Apoptosis plays an important role in the occurrence and development of ALI, which is involved in lung tissue injury and promoting the development of ALI.

       

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