摘要
目的探讨急性肺损伤时支气管肺泡灌洗液（BALF）中的中性粒细胞（PMN）凋亡发生规律及其与粒细胞集落刺激因子调控关系。方法豚鼠30只，分为3组：纽1为生理盐水正常对照组，纽2为油酸致病组，组3为油酸＋粒细胞集落刺激因子组。组2、组3分别由尾静脉注射油酸（0．12mL／kg）造成豚鼠急性肺损伤模型。组1则注入生理盐水。组3在实验造模前2d由皮下注射粒细胞集落刺激因子1．0μg／kg，1次／d。组1、组2、组3分别于注射后2h用生理盐水进行全肺支气管肺灌洗，收集BALF。用梯度密度法离心收集PMN。用原位末端标记法检测BALF中PMN凋亡。结果组2、组3和组1BALF中PMN凋亡百分比分别为（2．500±1．080）％、（3．500±0．850）％、（6．400±1．505）％。组2、组3较组1BALF中PMN凋亡均显著降低（均P〈0．01）。结论，急性肺损伤炎性细胞PMN凋亡延迟，PMN持续激活和释放毒性内容物与肺损伤有密切关系。粒细胞集落刺激因子能调控干预急性肺损伤时PMN凋亡延迟。
Objective To investigate the apoptosis of poly morphonuelear neutrophil （PMN） and the reversion of recombinant human granuloeyte colony-stimulating factor（G-CSF） in acute lung injury. Methods 30 guinea pigs were randomly divided into three groups ： control group, oil acid group （ OA group ） , OA ＋ G-CSF group. Both OA group and OA ＋ G-CSF group had intraveneos injection of oleie acid （0.12ml/kg） to induce acute lung injury. OA ＋ G-CSF group had G-CSF 0.5 μg/kg injection once a clay for 2 days. Control group had injection of normal saline. All the 3 groups took BALF 2 hours later. PMNs were isolated by density gradient eentrifugation. PMN apoptosis was detecded by Terminal deoxynucleotidy transferase-mediated dUTP biotin nick end labeling （TUNEL）. Results PMN apoptosis Of BALFs of OA group, OA ＋ G-CSF group and control group were （ 2.5 ± 1. 080） %, （ 3.5 ± 0. 850 ） % and（6.4 ± 1. 505） %. The level of PMN apoptosis of BALF of OA group compared with OA ＋ G-CSF group and control group were decreased markedly （ P 〈 0.01 for each）. Conclusion The apoptosis of PMN in acute lung injury is delayed, and persistent activation of PMN and release of toxic content is closely related to lung injury. G：CSF can reverse the level of apoptosis of PMN in acute lung injury.
出处
《中国综合临床》
北大核心
2008年第5期431-432,共2页
Clinical Medicine of China
基金
黑龙江省自然科学基金项目（D0313）
关键词
急性肺损伤
粒细胞集落刺激因子
Acute lung injury
Granulocyte colony-stlmulating factor
