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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）。
AIM: To investigate the protective effect of dexamethasone on activation-mediated PMN impairment. Methods: ZNHS was used in human PMN and PMN in mice to select the concentration and time of dexamethasone (Dex) for protective effect. In vitro and in vivo protective efficacy tests were conducted. Results: (1) Pretreatment with low dose Dex (0.08μg / ml) had no significant protective effect on functional damage of PMN in normal people and rats with ZAHS with very high dose; high dose Dex (1.2-1.6μg / ml) (P <0.05), but then the PMN cells died and shed off. The moderate dose of Dex (0.4 ~ 0.8μg / ml) could make the ICN of PMN , O-2 and SG levels were significantly higher than the experimental group (P <0.05); ②Dex in mice in vivo protective efficacy was consistent with in vitro experiments; ③Dex critical protection dose: 0.4μg / ml (in vitro ) Or 2.5 [mu] g / 20 g of rat (in vivo). The protective efficacy against PMN was 25.03% (in vitro) and 19.05% (in vivo), respectively. CONCLUSION: Pretreatment of medium PMN with a moderate amount of Dex (0.4 ~ 0.8μg / ml) can significantly and safely protect the intracellular bactericidal activity of PMNs stimulated by ZAHS. The conditions in the mice were essentially the same in vitro (2.5 μg / 20 g dose of Dex in vivo and 0.5 ml / 20 g mice for ZAMS).