雷公藤氯内酯醇对急性肺损伤核因子-κB的调节功能观察

Observation on regulative function of tripchrolide(雷公藤氯内酯醇) to nuclear factor-kappa B activation in acute lung injury patients

目的 :探讨核因子κB(NFκB)在急性肺损伤 (AL I)中的作用及雷公藤氯内酯醇 (T4 )的调节功能。方法 :实验分 AL I组、雷公藤 T4 组、健康对照组。用迁移电泳法 (EMSA)检测外周血单核细胞 (PBMC)中NFκB活性 ;用酶联免疫吸附法 (EL ISA)检测 PBMC培养上清中肿瘤坏死因子α(TNFα)、白细胞介素 10(IL 10 )含量。结果 :与健康对照组比较 ,AL I组 PBMC中 NFκB活性明显增强 (P<0 .0 1) ,PBMC培养上清中 TNFα、IL 10含量均明显升高 (P均 <0 .0 1) ;TNFα含量随 NFκB活化而增高 ,两者呈显著正相关(r=0 .79,P<0 .0 1)。与 AL I组比较 ,雷公藤 T4 组 PBMC中 NFκB活性显著下降 (P<0 .0 1) ;TNFα、IL 10含量亦明显下降 (P<0 .0 5和 P<0 .0 1)。结论 :AL I时 PBMC中 NFκB明显活化 ,介导促炎、抗炎介质大量释放 ,参与 AL I发生。雷公藤 T4 能明显抑制 NFκB活化及促炎介质 TNFα、抗炎介质 IL 10释放 ,调节促炎 /抗炎反应失衡。

Objective: To investigate the potential role of nuclear factor-kappa B((NF-κB) activation with acute lung injury(ALI) patients and the regulative function of tripchrolide(雷公藤氯内酯醇,T 4). Methods: Patients were randomly divided into ALI group, T 4 group and control group. NF-κB activity of the peripheral blood mononuclear(PBMC) were detected by electrophoresis mobility shift assay(EMSA). The concentration of tumor necrosis factor-α (TNF-α) and interleukin-10(IL-10) levels in the supernatant were measured by enzyme linked immunoadsorbent assay(ELISA) respectively. Results: Compared to the control group, the activity of NF- κB significantly increased in ALI group (P<0.01), the level of TNF-α and IL-10 in the PBMC supernatant also elevated markedly (both P<0.01). The relation analysis showed that the value of TNFα had significantly positive relation with that of NF- κB(r=0.79,P<0.01). Compared to the ALI group, the activity of NF-κB in PBMC and the level of TNF-α and IL-10 in T 4 group significantly decreased( P<0.01,P<0.05, P<0.01 respectively). Conclusion: The activation of NF-κB in ALI patients is up-regulate inflammatory mediator TNF-α and anti-inflammatory mediator IL10 expression which participate in ALI. The activity of NF-κB and pro-inflammatory mediator TNF-α and anti-inflammatory mediator IL-10 can be depressed markedly by tripchrolide, which restore the balance of pro-inflammatory response/anti-inflammatory response.