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目的探讨大鼠肺泡巨噬细胞(AM)在老年多器官功能衰竭(MOFE)肺启动形成过程中的作用。方法用酵母多糖腹腔注射复制大鼠MOFE模型。实验动物分为老年模型组、老年对照组、青年模型组和青年对照组4组,每组6只鼠。通过支气管肺泡灌洗和细胞贴壁的方法获取AM,用碘化丙啶染色流式细胞仪测定AM凋亡百分率,用Fluo3AM和Rhodamine123染色流式细胞仪测定AM胞内钙、线粒体膜电位。结果老年模型组AM凋亡率明显高于青年模型组(分别为434%±84%和242%±30%,P<001)。模型组与对照组相比,胞内游离钙浓度增加,而线粒体膜电位△Ψm降低。结论老年MOFE大鼠模型的AM的凋亡率大于青年大鼠模型,这可能是MOFE肺部感染后炎症不易控制以及肺部感染或肺损伤后容易引起MOFE的重要原因。AM胞内Ca2+浓度和线粒体膜电位的改变很可能是导致AM凋亡增加的重要原因。
Objective To investigate the role of rat alveolar macrophages (AMs) in the development of pulmonary organ in senile multiple organ failure (MOFE). Methods The rat model of MOFE was made by intraperitoneal injection of zymosan. The experimental animals were divided into four groups: the aged model group, the aged control group, the young model group and the young control group, with 6 rats in each group. AM was obtained by bronchoalveolar lavage and cell adherent method. AM apoptosis percentage was measured by propidium iodide staining flow cytometry. Intracellular calcium and mitochondrial membrane potential were measured by Fluo3AM and Rhodamine123 staining flow cytometry. Results The apoptosis rate of AM in aged model group was significantly higher than that in young model group (434% ± 84% and 242% ± 30%, P <001 respectively). Compared with the control group, the intracellular free calcium concentration increased and the mitochondrial membrane potential △ Ψm decreased in model group. Conclusion The apoptotic rate of AM in aged MOFE rat model is higher than that in young rat model. This may be the reason that MOFE is easily controlled by the inflammation after MOFE pulmonary infection and easily lead to MOFE after pulmonary infection or lung injury. AM intracellular Ca2 concentration and mitochondrial membrane potential changes is likely to lead to an important reason for the increase in AM apoptosis.