【摘要】 目的 制备小鼠肾炎模型并观察双氢青蒿素（dihydroartemisinine，DHA）对模型小鼠细胞因子肿瘤坏死因子-α（tunor necrosis factor，TNF-α）和白细胞介素-6（inter leukin-6，IL-6）的影响以及小鼠肾脏的病理变化。 方法 取雄性昆明种小鼠120只， 随机分为正常对照组、脂多糖（lipopolysaccharides，LPS）组、LPS+肾匀浆组及DHA治疗组；分别于12、24、48 h取血，酶联免疫吸附试验检测血清中TNF-α和IL-6的含量，苏木精-伊红染色法观察小鼠肾脏的病理变化。 结果 造模48 h LPS+肾匀浆组小鼠肾小球出现炎性细胞浸润，而正常对照组未见异常；LPS组及 DHA治疗组仅有轻微的病理改变。LPS刺激使小鼠血清TNF-α和IL-6含量高于正常水平（Plt;0.01），但有随时间不断下降的趋势；LPS+肾匀浆组较正常对照组TNF-α和IL-6含量升高（Plt;0.01）；DHA可显著下调模型小鼠血清TNF-α的水平（Plt;0.01），但对IL-6的影响相对较小（Pgt;0.05）。 结论 运用改良的造模方法LPS+肾匀浆建立肾炎模型效果良好；DHA可以调节模型小鼠炎症因子TNF-α和IL-6的释放，具有一定的改善模型小鼠肾炎症状的作用。【Abstract】 Objective To establish mice nephritis models, detect the serum level changes of cytokines tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in the model mice treated by Dihydroartemisinin (DHA), and observe the physiological changes of the mice kidneys. Methods One hundred and twenty male Kunming mice were randomly divided into 4 groups: control group, lipopolysaccharides (LPS) group, LPS plus kidney homogenate group, and DHA treated group. The level of cytokines TNF-α and IL-6 in the serum were detected by enzyme-linked immunoabsordent assey at hour 12, 24, and 48, respectively. Pathological changes were observed by hematoxylin: eosin staining. Results At the time hour 48 after the establishment of the model, inflammatory cell infiltration was observed in the glomerulus of the LPS plus kidney homogenate group, but no abnormality was found in the control group. There were only slight pathological changes in mice models of the LPS group and the DHA treated group. The serum level of TNF-α and IL-6 increased remarkably after the treatment of LPS (Plt;0.01), but declined as time went by. The level of TNF-α and IL-6 increased significantly in LPS plus kidney homogenate group compared with the control group (Plt;0.01). DHA could significantly decrease the TNF-α level in the serum (Plt;0.01), but had a low influence on IL-6 (Pgt;0.05). Conclusion The modified LPS plus kidney homogenate has a good result in model establishing. DHA can regulate the release of TNF-α and IL-6 in the model mice, and may have certain good effects on ameliorating the nephritis pathological changes.