摘要
目的:研究地塞米松对活化补体介导的PMN功能损害的保护作用。方法:用酵母多糖活化人血清(ZAHS)作用于人体外PMN及小鼠体内PMN,选择地塞米松(Dex)起显著保护作用的浓度和时间;进行体内、外保护效能试验。结果:①低剂量Dex(0.08μg/ml)预处理,对极效量ZAHS导致正常人、鼠PMN功能损害无明显保护作用;大剂量Dex(1.2~1.6μg/ml)在PMN应激后的第5小时前表现出明显保护作用(P<0.05),但此后却使PMN细胞死亡、脱落;中等剂量Dex(0.4~0.8μg/ml)能使PMN的ICBA、O-2和SG三项指标水平均显著高于实验组(P<0.05);②Dex在小鼠体内保护效能同体外实验基本一致;③Dex的临界保护剂量:0.4μg/ml(体外)或2.5μg/20g鼠(体内),它对PMN杀菌力的保护效能分别为25.03%(体外)和19.05%(体内)。结论:中等量Dex(0.4~0.8μg/ml)对体外PMN的预处理,能显著而安全地保护ZAHS所激化的PMN的胞内杀菌功能。鼠体内的情况基本同体外一致(体内Dex剂量为2.5μg/20g小鼠,ZAMS为0.5ml/20g小鼠)。
Objective: To investigate the protective effects of dexamethosone on damage of polymorphonuclear neutrophils (PMNs) induced by the activated complement. Methods: The zymosanactivated human serum (ZAHS) was added to monolayer culture of human PMNs and injected into the murine body to determine the optimal protective dose and time of dexamethasone and test its protective efficiency in vivo and in vitro. Results: 1) Pretreatment of low dose of dexamethasone (0.08 μg/ml) could not exert significant protective effects on ZAHSdisturbed PMNS while that of high dose of dexamethasone (1.2~1.6 μg/ml) could within 5 hours after treatment (P<0.05). However, the latter soon caused the death and falling off of PMNs. Pretreatment of middle dose of dexamethasone (0.4~0.8 μg/ml) could preserve ICBA, O-2 and SG to levels significantly higher than those in the experimental group (P<0.05). 2) The protective effects exerted in the murine body were consistent with those in vitro. 3) The critical protective dose of dexamethasone was 0.4 (g/ml in vitro or 2.5 μg/20g in vivo and its protective efficiency to ICBA was 25.03% in vitro or 19.05% in vivo. Conclusion: Pretreatment of PMNs with middle dose of dexamethasone can significantly and safely protect ICBA of PMNs from the disturbance of ZAHS.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1997年第6期523-526,共4页
Journal of Third Military Medical University
关键词
地塞米松
补体
杀菌力
烧伤
并发症
感染
PMN
dexamethasone
complement
bactericidal
superoxide ion
specific granule