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

被引:21
作者
Yu, Tianliang [1 ]
Xie, Weili [1 ]
Sun, Yu [1 ]
机构
[1] Harbin Med Univ, Clin Hosp 1, Harbin 150001, Heilongjiang, Peoples R China
关键词
Oridonin; LPS; Human gingival fibroblasts; IL-6; PPAR gamma; NF-KAPPA-B; ACUTE LUNG INJURY; RECEPTOR-GAMMA; BONE LOSS; GENE-EXPRESSION; LIPOPOLYSACCHARIDE; ROSIGLITAZONE; PERIODONTITIS; AGONISTS; ACID;
D O I
10.1016/j.intimp.2019.04.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 mu g/mL) was administrated 1 h before LPS treatment. The results showed that oridonin significantly inhibited inflammatory mediators PGE(2), NO, IL-6, and IL-8 production. Immunoblotting experiments revealed that oridonin reduced the expression of phosphorylation levels of NF-kappa B p65 and I kappa B alpha. Furthermore, the expression of PPAR gamma was up-regulated by the treatment of oridonin. Further studies showed that PPAR gamma inhibitor GW9662 could reverse the inhibition of oridonin on PGE(2), NO, IL-6, and IL-8 production. In conclusion, oridonin inhibited LPS-induced microglia activation through activating PPAR gamma.
引用
收藏
页码:301 / 307
页数:7
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