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目的 探讨一氧化氮 (NO)和白介素 - 10 (IL - 10 )对内毒素 (LPS)诱导的肺泡巨噬细胞核因子 -κB(NF -κB)活化的调节 ,为临床运用提供理论依据。方法 用支气管肺泡灌洗法收集肺泡巨噬细胞 (PAM)进行培养 ,分正常对照组、LPS组、NO +LPS组和IL - 10 +LPS组。用凝胶电泳迁移率改变分析 (EMSA)法和ELISA法分别检测提取物中NF -κB活性和细胞培养上清中TNF -α含量。结果 LPS组NF -κB活性和TNF -α含量在刺激后 0 5～ 4h显著高于正常对照组 (P <0 0 1) ;NO+LPS组和IL - 10 +LPS组的NF -κB活性和TNF -α含量与LPS组相比均明显下降 ,尤在刺激后 1h最显著 (P <0 0 1)。结论 LPS诱导PAM的NF -κB活化 ,导致TNF -α基因表达增强 ;NO和IL - 10可抑制NF -κB活化 ,减少TNF -α的释放 ,缓解LPS诱导的ALI。
Objective To investigate the regulation of nitric oxide (NO) and interleukin - 10 (IL - 10) on the activation of nuclear factor - κB (NF - κB) induced by endotoxin (LPS) in alveolar macrophages, and to provide a theoretical basis for its clinical application. Methods Alveolar macrophages (PAMs) were collected by bronchoalveolar lavage and cultured in normal control, LPS, NO + LPS and IL - 10 + LPS groups. The activity of NF-κB in the extract and the content of TNF-α in the cell culture supernatant were detected by EMSA and ELISA respectively. Results The levels of NF-κB and TNF-α in LPS group were significantly higher than those in normal control group from 0-5 h to 4 h after stimulation (P <0.01). The activity of NF-κB in NO + LPS group and IL - 10 + LPS group Compared with LPS group, the content of TNF-α decreased significantly, especially at 1 hour after stimulation (P <0.01). CONCLUSION: LPS induces the activation of NF-κB in PAM, leading to the enhancement of TNF-α gene expression. NO and IL-10 can inhibit the activation of NF-κB, decrease the release of TNF-α and alleviate LPS-induced ALI.