目的 体外考察蠲痹历节清方抗痛风炎症作用及其分子机制。方法 利用单钠尿酸盐( MSU)结晶诱导巨噬细胞建立体外痛风模型，用蠲痹历节清方(44 g·kg^-1)大鼠含药血清(10%)，以及PPARγ激动剂吡格列酮20 μmol·L^-1、NF-κB阻断剂SN50 20 μmol·L干预，酶联免疫法测定TNF-α、IL-1β、IL-6含量，RT-PCR法与Western-Blot法分别检测PPARγ、TLR4基因转录及蛋白表达，免疫荧光法考察NF-κB核移位。结果 与正常对照组比较，MSU诱导巨噬细胞TNF-α、IL-1β、IL-6水平均显著增加(P < 0.01)，PPARγ基因转录与表达显著降低(P < 0.01)，TLR4基因转录与表达显著增加(P < 0.01)，NF-κB核移位。与模型组比较，蠲痹历节清方含药血清，可显著降低TNF-α、IL-1β、IL-6水平(P < 0.01)，增加PPARγ基因转录与表达(P < 0.01)，降低TLR4基因转录与表达(P < 0.01)，阻止NF-κB核移位，其作用与吡格列酮相似。SN50对PPARγ无影响。结伦 蠲痹历节清方可能部分通过上调巨噬细胞PPARγ，抑制TLR4/NF-κB信号通路，抑制痛风炎症反应。

Objective To investigate the anti-gout inflammation effects of Juanbillijieqing Formula and its molecular mechanism in vitro.Methods Firstly, macrophages were induced by crystallization of monosodium urate (MSU) to establish gout model in vitro. Then, the drug-containing serum (10%) of Juanbillijieqing Formula (44 g·kg^-1) rats, the PPARγ agonists (pioglitazone, 20 μmol·L^-1) and NF-κB blocker (SN50 20 μmol·L^-1) were used for intervention. The content of TNF-α, IL-1β and IL-6 was determined by ELISA. The transcriptions and protein expressions of PPARγ and TLR4 genes were detected respectively by RT-PCR and Western-Blot. The nuclear translocation of NF-κB was investigated by immunofluorescence assay.Results Compared with the normal control group, the levels of TNF-α, IL-1β and IL-6 in MSU induced macrophages were increased significantly (P < 0.01); the transcription and expression of PPARγ gene were decreased significantly (P < 0.01); the transcription and expression of TLR4 gene were increased significantly (P < 0.01); and the nucleus of NF-κB was translocated. Compared with the model group, the serum containing Juanbillijieqing Formula could significantly reduce the levels of TNF-α, IL-1β and IL-6 (P < 0.01), increase the transcription and expression of PPARγ gene (P < 0.01), decrease the transcription and expression of TLR4 gene (P < 0.01), and prevent the nuclear translocation of NF-κB. Its effects were similar to those of pioglitazone. SN50 had no effect on PPARγ.Conclusion Juanbillijieqing Formula may partially inhibit gouty inflammation by up-regulating PPARγ in macrophages and inhibiting TLR4/NF-κB signaling pathway.