TLR4型
化学
炎症
MAPK/ERK通路
信号转导
一氧化氮
肿瘤坏死因子α
NF-κB
p38丝裂原活化蛋白激酶
脂多糖
细胞生物学
生物化学
药理学
生物
免疫学
有机化学
作者
Eui‐Baek Byun,Nak-Yun Sung,Eui-Hong Byun,Du-Sup Song,Jae‐Kyung Kim,Jong-Heum Park,Beom‐Seok Song,Sang‐Hyun Park,Ju-Woon Lee,Myung‐Woo Byun,Jae‐Hun Kim
标识
DOI:10.1016/j.intimp.2012.11.021
摘要
Natural products and dietary components rich in polyphenols have been shown to reduce inflammation; however, the molecular mechanisms underlying this anti-inflammatory activity are not completely characterized, and many features remain to be elucidated. This research was carried out to clarify the potential role of procyanidin trimer C1 in the anti-inflammatory effect of polyphenols. Procyanidin C1 inhibited inducible nitric oxide synthase-mediated nitric oxide production and the release of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) in lipopolysaccharide (LPS)-induced macrophages. Treatment with procyanidin C1 resulted in a significant decrease in prostaglandin E2 and cyclooxygenase-2 levels, as well as the expression of cell surface molecules (CD80, CD86, and MHC class II), which was induced by LPS. Furthermore, our data demonstrated that the anti-inflammatory effect of procyanidin C1 occurs through inhibition of mitogen-activated protein kinase (p38 and c-Jun N-terminal kinase) and nuclear factor-κB signaling pathways. These 2 factors play a major role in controlling inflammation, through toll-like receptor 4, suggesting that procyanidin C1 plays a potent role in promoting anti-inflammatory activity in macrophages. These results represent a novel and effective therapeutic intervention for the treatment of inflammatory disease.
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