目的 研究中药地黄饮子抑制脂多糖（LPS）诱导的小胶质细胞炎症反应的作用机制。方法 使用1 mg·L^-1的LPS诱导小鼠小胶质细胞系（BV2）构建细胞炎症模型，实验分组为空白组、模型组、地黄饮子组（14.5 g·kg^-1）、米诺环素组（150 mg·kg^-1）。地黄饮子组和米诺环素组予以10%的含药血清干预，空白组和模型组给予同等浓度的空白血清。明场下观察细胞形态的变化，实时荧光定量PCR检测促炎性因子IL-1β、IL-6、TNF-α mRNA表达水平，Western blot检测PPARγ蛋白表达和NF-κB p65活化水平，细胞免疫荧光检测NF-κB p65入核情况。结果 与空白组比较，模型组促炎性因子IL-1β、IL-6、TNF-α的mRNA水平均显著升高（P < 0.01）；PPARγ蛋白水平明显降低，NF-κB磷酸化水平明显增高，差异均有统计学意义（P <0.01），LPS刺激使BV2细胞核内NF-κB含量明细增多；给予地黄饮子或米诺环素含药血清干预后，与模型组比较，炎性因子IL-1β、IL-6、TNF-α的 mRNA 水平均显著降低（P < 0.05），PPARγ蛋白水平明显升高（P < 0.05），NF-κB磷酸化水平和入核含量明显减少（P < 0.05）。结论 地黄饮子可能通过调控PPARγ/NF-κB信号通路抑制LPS诱导的BV2细胞炎症反应。

Objective To investigate the inhibitory effect of Dihuang-Yinzi Decoction on LPS induced inflammatory reaction and its specific mechanism.Methods The inflammation model of BV2 cell was induced by LPS. The cultured cells were divided into: blank group, model group, Dihuang-Yinzi group, and minocycline group. The Dihuangyinzi group and minocycline group were intervened with 10% medicated serum, and the blank group and model group were given the same concentration of blank serum. Real time PCR was used to detect the mRNA expression of pro-inflammatory factors IL-1β, IL-6 and TNFα. Western blotting was used to detect the expression of PPARγ and the activation of NF-κBp65 in BV2 cells. Immunofluorescence was used to detect the nuclear entry of NF-κBp65.Results Compared with the blank group, the mRNA levels of proinflammatory cytokines IL-1β, IL-6 and TNFαin the LPS model group were significantly increased (P < 0.01). PPAR γ protein level was significantly decreased, and NF-κ B phosphorylation level was significantly increased (P < 0.01). LPS stimulation increased the nuclear content of NF-κ B in BV2 cells. After intervention with Dihuangyinzi or minocycline medicated serum, the mRNA levels of inflammatory factors IL-1 β, IL-6 and TNF-α were significantly lower than those in the model group (P< 0.05), the protein level of PPAR γ was significantly higher than that in the model group (P < 0.05), and the phosphorylation level and nuclear content of NF-κ B were significantly lower than those in the model group (P < 0.05).Conclusion Dihuangyinzi can inhibit LPS-induced inflammatory response of BV2 cells, and its specific mechanism may be related to thePPAR γ/NF-κB signaling pathway.

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