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目的：探讨雷公藤单体雷公藤氯内酯醇(trip-cholorolide,T4)对肺泡巨噬细胞(AM)炎症反应的影响及机制.方法：小鼠AM受脂多糖(LPS)lO mg/L刺激的同时，加入T4 500μg/L或地塞米松100μmol/L；ELISA法测定上清液中TNFα、IL-lβ、IL-6及IL-10浓度；RT-PCR检测上述因子及iNOS基因mRNA的表达.结果：AM受10 mg/LPS刺激24小时后，上清液中TNFα、IL-lβ、IL-6、IL-10及NO释放均明显增加.T4 500μg/L及地塞米松100μmol/L对上述介质均有不同程度的抑制作用.LPS刺激5小时后，AM中TNFα、IL-6、IL-10和iNOS的mRNA表达均明显增加.T4和地塞米松对上述介质的mRNA表达均有明显抑制作用.另外，T4对TNFα、IL-6、IL-10 mRNA的稳定性无明显影响.结论：T4具有抑制AM中促炎介质和抗炎介质表达的作用.“,”AIM: To observe the effects of tripcholorolide (T4) on inflammatory reaction of mouse alveolar macrophages.METHODS: RT-PCR was used to investigate tumor necrosis factor α (TNFα), interleukin-lβ (IL-lβ), IL-6, IL-10, and inducible nitric-oxide synthase (iNOS) mRNA expression in alveolar macrophages after LPS 10 mg/L and T4 500μg/L treaunent. ELISA was used to detect TNFα, IL-lβ, IL-6, and IL-10 protein expression. Nitrite was measured by Griess reaction. RESULTS: TNFα, IL-lβ, IL-6, IL-10, and nitrite increased in supematants, when alveolar macrophages were stimulated by LPS 10 mg/L at 24 h. Both T4 500 μtg/L and dexamethasone 100μmol/L had inhibitory effects on the production of TNFα, IL-lβ, IL-6, IL-10, and nitric oxide. The mRNA expression of TNFα, IL-6, IL-10, and iNOS increased at 5 h after LPS stimulation which was decreased on addition of T4 500 μg/L or dexamethasone 100μmol/L. T4 had no effect on stability of LPS-induced mRNA expression in TNFα, IL-6, and IL-10.CONCLUSION: T4 had inhibitory effects on the expression of proinflammatory and antiinflammatory mediators.