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首页> 外文期刊>Digestive Diseases and Sciences >Quercetin Attenuates Adhesion Molecule Expression in Intestinal Microvascular Endothelial Cells by Modulating Multiple Pathways
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Quercetin Attenuates Adhesion Molecule Expression in Intestinal Microvascular Endothelial Cells by Modulating Multiple Pathways

机译：槲皮素通过调节多种途径衰减肠道微血管内皮细胞中的粘附分子表达

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BackgroundIn inflammatory bowel disease, activation of microvascular endothelial cells and adhesion of immune cells are required for the initiation and maintenance of inflammation. We evaluated the effects and mechanisms of quercetin, a flavone identified in a wide variety of dietary sources, in LPS-induced rat intestinal microvascular endothelial cells (RIMVECs).MethodsRIMVECs were pretreated with quercetin of various concentrations (20, 40 and 80M) followed by LPS (10g/ml) stimulation. ELISA was used to examine protein levels of intercellular adhesion molecules-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the supernatant. Protein levels of Toll-like receptor 4 (TLR4), nuclear transcription factor kappa B (NF-B) p65, inhibitors of NF-B (IB-), extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK) p38 and signal transducer and activator of transcription (STAT) in cells were measured by Western blot.ResultsQuercetin significantly suppressed protein levels of ICAM-1 and VCAM-1 induced by LPS. Quercetin also inhibited TLR4 expression, NF-B p65, ERK, JNK and STAT phosphorylation and decreased IB- degradation. Moreover, the MAPK p38 signal does not contribute to the anti-inflammatory effects on RIMVECs, although LPS significantly increases its phosphorylation.ConclusionsThese results indicate that quercetin may have an anti-inflammatory effect by inhibiting expression of ICAM-1 and VCAM-1 in RIMVECs by suppressing TLR4, NF-B, ERK, JNK and STAT but not the p38 signaling pathway.
机译：背景炎性肠病，炎症的开始和维持炎症的激活和免疫细胞的粘附。我们评估了槲皮素，在LPS诱导的大鼠肠道微血管内皮细胞（RIMVECs）中鉴定的一种膳食源中鉴定的黄酮的影响和机制.Methodsrimvecs用各种浓度（20,40和80m）的槲皮素预处理LPS（10g / ml）刺激。使用ELISA检查上清液中细胞间粘附分子-1（ICAM-1）和血管细胞粘附分子-1（VCAM-1）的蛋白质水平。 Toll样受体4（TLR4），核转录因子Kappa B（NF-B）P65，NF-B（IB-）的抑制剂，细胞外信号调节激酶（ERK），C-JUN N-末端激酶（JNK），通过Western Blot测量细胞中的丝肠激活蛋白激酶（MAPK）P38和信号传感器和信号传感器（STAT）的转录（统计）测量蛋白质显着抑制了LPS诱导的ICAM-1和VCAM-1的蛋白质水平。槲皮素还抑制TLR4表达，NF-B P65，ERK，JNK和统计磷酸化并降低IB-降低。此外，MAPK P38信号对RIMVEC的抗炎作用没有有助于对RIMVEC的抗炎作用，尽管LPS显着增加其磷酸化。结论，结果表明槲皮素可以通过抑制RIMVEC的ICAM-1和VCAM-1的表达具有抗炎作用通过抑制TLR4，NF-B，ERK，JNK和统计而不是P38信令路径。

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