摘要
目的：探讨巨噬细胞在烧伤后免疫功能紊乱中的作用机制。方法：通过比色法及放免法分别测定体外小鼠腹腔巨噬细胞培养上清中ＮＯ及ＰＧＥ２的含量，并通过在培养体系中加入消炎痛、Ｌ－精氨酸、ＮＭＭＡ等影响ＰＧＥ２及ＮＯ的产生，以同位素掺入法观察它们在烧伤后ＰＭ抑制ＣｏｎＡ刺激的ＳＰＬ增殖反应中的作用。结果：烧伤早期巨噬细胞就具有产生大量ＮＯ和ＰＧＥ２的能力。在ＰＭΦ与ＳＰＬ共同培养中发现，烧伤后巨噬细胞能明显抑制ＳＰＬ的增殖，其抑制率高达８２．３％。消炎痛使抑制率下降到６２．３％，但Ｌ－精氨酸能明显增强此抑制作用，而ＮＭＭＡ能减弱此抑制作用，并且消炎痛与ＮＭＭＡ有相互叠加的作用。结论：烧伤后巨噬细胞能通过产生ＮＯ及ＰＧＥ２而抑制机体的细胞免疫功能。
Objective: To investigate the mechanism of
immune dysfunction after burn injury. Methods: NO and PGE2 in the supernatant of the
cultured peritoneal macrophages (PM) were determined with colorimetric and RIA method
respectively. The proliferation of stimulated splenic lymphocytes (SPL) cocultured with PM was
detected by 3HTdR incorporation. Results: NO production form PM was increased rapidly after
the burns, which began to reach a significantly higher level since PB 6 h and persisted at a
high level till PB 48 h. PGE2 production was markedly increased from PB 24 h. The coculture of
the two kinds of cells showed that PM from PB 24 h mice could remarkably inhibit the
proliferation of normal SPL stimulated by Con A. Larginine and NMMA could upregulate and
downregulate this suppression respectively. Indomecine, a specific blocker of cyclooxygenase,
also markedly attenuated the Con Astimulated SPL proliferation. Conclusion: NO and PGE2
derived from PM play an important role in the immune dysfunction after burns.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1999年第5期335-337,共3页
Journal of Third Military Medical University
基金
国家自然科学基金
