活力测定
TLR4型
趋化因子
分子生物学
脐静脉
人脐静脉内皮细胞
CXCL10型
炎症
白细胞介素8
CCL5
Toll样受体
单核细胞
促炎细胞因子
生物
受体
化学
细胞凋亡
免疫学
T细胞
先天免疫系统
免疫系统
生物化学
白细胞介素2受体
体外
作者
Liyong Chen,Yu Cx,Bao‐Hua Song,Weimin Cai,Liu C,Guan Qb
出处
期刊:PubMed
日期:2018-04-01
卷期号:22 (8): 2421-2431
被引量:7
标识
DOI:10.26355/eurrev_201804_14835
摘要
To investigate the role of Toll-like receptor-4 (TLR4) in the free fatty acids (FFAs) induced human umbilical vein endothelial cells (HUVECs) inflammation and to explore the underlying mechanisms.HUVECs and HEK293 cell lines were obtained from Shanghai Type Culture Collection. Cell counting kit-8 (CCK8) and flow cytometry (FCM) were performed to examine the cell viability and apoptosis rate of HUVECs induced by FFAs treatments with or without infection of toll-like receptor-4 interference (TLR4i) adenovirus. Enzyme-linked immunosorbent assay (ELISA) was performed to evaluate the inflammatory cytokines release. Quantitative polymerase chain reaction (qPCR) and Western Blot (WB) were used to test the molecular mechanisms of inflammation.FFAs induced inflammatory responses in HUVECs via modulating the TLR4 receptor complex. TLR4i adenovirus interference increased cell viability and decreased cell apoptosis rate. FFAs treatments significantly increased the expressions of inflammatory cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), C-C motif chemokine ligand 5 (CCL5) and CXC chemokine ligand 10 (CXCL10), while TLR4i adenovirus interference significantly reduced these cytokines levels. TLR4-mediated myeloid differential protein-88 (MyD88) expression activating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and inhabiting kappa B kinase-beta (IKK-β). TLR4i adenovirus interference decreased the expressions of these genes at both mRNA level and protein level.TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.
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