中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2008年
5期
431-432
,共2页
韩守信%陈复辉%周丹%吴晓梅
韓守信%陳複輝%週丹%吳曉梅
한수신%진복휘%주단%오효매
急性肺损伤%粒细胞集落刺激因子
急性肺損傷%粒細胞集落刺激因子
급성폐손상%립세포집락자격인자
Acute lung injury%Granulocyte colony-stimulating factor
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:组1为生理盐水正常对照组,组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(0.12 ml/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2 d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2 h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1 BALF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.
目的 探討急性肺損傷時支氣管肺泡灌洗液(BALF)中的中性粒細胞(PMN)凋亡髮生規律及其與粒細胞集落刺激因子調控關繫.方法 豚鼠30隻,分為3組:組1為生理鹽水正常對照組,組2為油痠緻病組,組3為油痠+粒細胞集落刺激因子組.組2、組3分彆由尾靜脈註射油痠(0.12 ml/kg)造成豚鼠急性肺損傷模型.組1則註入生理鹽水.組3在實驗造模前2 d由皮下註射粒細胞集落刺激因子1.0μg/kg,1次/d.組1、組2、組3分彆于註射後2 h用生理鹽水進行全肺支氣管肺灌洗,收集BALF.用梯度密度法離心收集PMN.用原位末耑標記法檢測BALF中PMN凋亡.結果 組2、組3和組1BALF中PMN凋亡百分比分彆為(2.500±1.080)%、(3.500±0.850)%、(6.400±1.505)%.組2、組3較組1 BALF中PMN凋亡均顯著降低(均P<0.01).結論 急性肺損傷炎性細胞PMN凋亡延遲,PMN持續激活和釋放毒性內容物與肺損傷有密切關繫.粒細胞集落刺激因子能調控榦預急性肺損傷時PMN凋亡延遲.
목적 탐토급성폐손상시지기관폐포관세액(BALF)중적중성립세포(PMN)조망발생규률급기여립세포집락자격인자조공관계.방법 돈서30지,분위3조:조1위생리염수정상대조조,조2위유산치병조,조3위유산+립세포집락자격인자조.조2、조3분별유미정맥주사유산(0.12 ml/kg)조성돈서급성폐손상모형.조1칙주입생리염수.조3재실험조모전2 d유피하주사립세포집락자격인자1.0μg/kg,1차/d.조1、조2、조3분별우주사후2 h용생리염수진행전폐지기관폐관세,수집BALF.용제도밀도법리심수집PMN.용원위말단표기법검측BALF중PMN조망.결과 조2、조3화조1BALF중PMN조망백분비분별위(2.500±1.080)%、(3.500±0.850)%、(6.400±1.505)%.조2、조3교조1 BALF중PMN조망균현저강저(균P<0.01).결론 급성폐손상염성세포PMN조망연지,PMN지속격활화석방독성내용물여폐손상유밀절관계.립세포집락자격인자능조공간예급성폐손상시PMN조망연지.
Objective To investigate the apoptosis of poly morphonuclear neutrophil(PMN)and the reversion of recombinant human granulocyte 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 oleic acid(0.12ml/kg)to induce acute lung injury.OA+G-CSF group had G-CSF 0.5μg/kg injection once a day 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 centrifugation.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.