Punicalagin Inhibits Inflammation in LPS-Induced RAW264.7 Macrophages via the Suppression of TLR4-Mediated MAPKs and NF-κB Activation

被引:216
作者
Xu, Xiaolong [1 ]
Yin, Peng [1 ]
Wan, Changrong [1 ]
Chong, Xinlu [2 ]
Liu, Mingjiang [1 ]
Cheng, Peng [2 ]
Chen, Jiajia [2 ]
Liu, Fenghua [1 ,2 ]
Xu, Jianqin [1 ]
机构
[1] China Agr Univ, Coll Vet Med, CAU BUA TCVM Teaching & Researching Team, Beijing 100193, Peoples R China
[2] Beijing Univ Agr, Coll Anim Sci & Technol, Beijing 102206, Peoples R China
关键词
punicalagin; anti-inflammation; proinflammatory cytokines; MAPKs; NF-kappa B; INDUCIBLE NO SYNTHASE; TOLL-LIKE RECEPTORS; POMEGRANATE JUICE; ANTIINFLAMMATORY ACTIVITY; THERAPEUTIC TARGET; OXIDATIVE STRESS; IMMUNE-RESPONSE; PROTEIN-KINASES; CELLS; MICE;
D O I
10.1007/s10753-014-9816-2
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Punicalagin (2,3,hexahydroxydiphenoyl-gallagyl-d-glucose and referred to as PUN) is a bioactive ellagitannin isolated from pomegranate, which is widely used for the treatment of inflammatory bowel disease (IBD), diarrhea, and ulcers in Chinese traditional medicine. In this study, we detected the anti-inflammation potentials of PUN in lipopolysaccharide (LPS)-induced macrophages and tried to uncover the underlying mechanism. Results demonstrated that PUN (25, 50, or 100 mu M) treatment could significantly decrease the LPS-induced production of nitric oxide), prostaglandin E-2 (PGE(2)), interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha in RAW264.7 cells. Molecular research showed that PUN inhibited the activation of upstream mediator nuclear factor-kappa B by suppressing the phosphorylation of I kappa B alpha and p65. Results also indicated that PUN could suppress the phosphorylation of mitogen-activated protein kinase including p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase. In conclusion, we observed that PUN could inhibit LPS-induced inflammation, and it may be a potential choice for the treatment of inflammation diseases.
引用
收藏
页码:956 / 965
页数:10
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