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冬凌草甲素通过激活 PPARγ 抑制 LPS 诱导的人牙龈成纤维细胞炎症。

Oridonin inhibits LPS-induced inflammation in human gingival fibroblasts by activating PPARγ.

机构信息

First Clinical Hospital of Harbin Medical University, Harbin 150001, China.

First Clinical Hospital of Harbin Medical University, Harbin 150001, China.

出版信息

Int Immunopharmacol. 2019 Jul;72:301-307. doi: 10.1016/j.intimp.2019.04.006. Epub 2019 Apr 18.

Abstract

Oridonin, the major terpene isolated from Rabdosia rubescens, has been used as dietary supplement. Recently, it has been known to exhibit anti-inflammatory effect. This study we employed an in vitro model of LPS-stimulated human gingival fibroblasts to investigate the anti-inflammatory effects and mechanism of oridonin. Oridonin (10-30 μg/mL) was administrated 1 h before LPS treatment. The results showed that oridonin significantly inhibited inflammatory mediators PGE, NO, IL-6, and IL-8 production. Immunoblotting experiments revealed that oridonin reduced the expression of phosphorylation levels of NF-κB p65 and IκBα. Furthermore, the expression of PPARγ was up-regulated by the treatment of oridonin. Further studies showed that PPARγ inhibitor GW9662 could reverse the inhibition of oridonin on PGE, NO, IL-6, and IL-8 production. In conclusion, oridonin inhibited LPS-induced microglia activation through activating PPARγ.

摘要

冬凌草甲素是从冬凌草中分离得到的主要萜类化合物,已被用作膳食补充剂。最近,它被认为具有抗炎作用。本研究采用脂多糖刺激的人牙龈成纤维细胞体外模型,探讨冬凌草甲素的抗炎作用及其机制。冬凌草甲素(10-30μg/ml)在 LPS 处理前 1 小时给药。结果表明,冬凌草甲素能显著抑制 PGE、NO、IL-6 和 IL-8 等炎症介质的产生。免疫印迹实验显示,冬凌草甲素降低了 NF-κB p65 和 IκBα 的磷酸化水平。此外,冬凌草甲素上调了 PPARγ 的表达。进一步的研究表明,PPARγ 抑制剂 GW9662 可逆转冬凌草甲素对 PGE、NO、IL-6 和 IL-8 产生的抑制作用。综上所述,冬凌草甲素通过激活 PPARγ 抑制 LPS 诱导的小胶质细胞激活。

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