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目的 探讨白介素 - 10对内毒素 (LPS)诱导肺泡巨噬细胞核因子 -κB(NF -κB)活化及肿瘤坏死因子α(TNF-α)基因表达的调节 ,为临床运用白介素 - 10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、IL - 10 +LPS组。用凝胶电泳迁移率改变分析 (EMSA)法和ELISA法分别检测核提取物中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明显高于正常对照组 ;IL -10 +LPS组NF -κB活性和TNF -α含量均显著低于LPS组。结论 LPS诱导PAM的NF -κB活化 ,导致TNF -α基因表达增强 ;白介素 - 10可抑制NF -κB活化而减少TNF -α的释放
Objective To investigate the regulation of interleukin - 10 on the activation of nuclear factor - κB (NF - κB) and the expression of tumor necrosis factor α (TNF - α) in alveolar macrophages induced by endotoxin (LPS), providing a theoretical basis for clinical application of interleukin - 10. Methods Alveolar macrophages (PAMs) were collected by bronchoalveolar lavage and cultured in normal control, LPS and IL - 10 + LPS groups. The activity of NF-κB in nuclear extracts and the content of TNF-α in cell culture supernatants 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 to 4 hours after stimulation. The levels of NF-κB and TNF-α in IL-10 + LPS group were significantly lower than those in LPS group. Conclusion LPS induces the activation of NF-κB in PAM, leading to the enhancement of TNF-α gene expression. Interleukin-10 inhibits the activation of NF-κB and decreases the release of TNF-α