期刊
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
卷 98, 期 6, 页码 357-365出版社
CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/cjpp-2019-0389
关键词
rhein; inflammation; RAW264.7 cells; lipopolysaccharide; NF-kappa B; PPAR-gamma
资金
- National Natural Science Foundation of China [81873162]
- Natural Science Foundation of Guangdong Province [2018B030 311014]
- Guangzhou Science and Technology Planning Project [201804010113]
Inflammation is a common inducer of numerous severe diseases such as sepsis. The NF-kappa B signaling pathway plays a key role in the inflammatory process. Its activation promotes the release of pro-inflammatory mediators like inducible nitric oxide synthase and tumor necrosis factor alpha. Peroxisome proliferator-activated receptor gamma (PPAR-gamma) inactivates nuclear factor kappa B (NF-kappa B) and subsequently attenuates inflammation. Rhein, an agent isolated from rhubarb, has been known to have anti-inflammatory effects. However, its influence on PPAR-gamma remains largely unknown. In this study, an inflammation model was constructed by stimulating RAW264.7 cells with lipopolysaccharide. Rhein was used as a therapeutic agent, while rosiglitazone (PPAR-gamma activator) and GW9662 (PPAR-gamma inhibitor) were used as disrupters for in depth studies. The results demonstrated that rhein inhibits NF-kappa B activation and inflammatory factor release. However, GW9662 significantly reduced this effect, indicating that PPAR-gamma is a critical mediator in the rhein-mediated anti-inflammatory process. Additionally, positive modulation of PPAR-gamma expression and activity by rosiglitazone correspondingly influenced the effects of rhein on inflammatory factors and NF-kappa B expression. We also found that rhein could enhance PPAR-gamma, NF-kappa B, and histone deacetylase 3 (HDAC3) binding. These results indicate that rhein exerts its anti-inflammation function by regulating the PPAR-gamma-NF-kappa B-HDAC3 axis.
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