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Isobavachalcone attenuates TNF-α-induced ICAM-1 and VCAM-1 expression in human umbilical vein endothelial cells by regulating the NF-κB signaling pathway
Applied Biological Chemistry ( IF 3.2 ) Pub Date : 2022-07-04 , DOI: 10.1186/s13765-022-00717-7 Lee, Ae Sin, Hur, Jinyoung, Choi, Sang Yoon
Applied Biological Chemistry ( IF 3.2 ) Pub Date : 2022-07-04 , DOI: 10.1186/s13765-022-00717-7 Lee, Ae Sin, Hur, Jinyoung, Choi, Sang Yoon
Vascular inflammation activated by pro-inflammatory cytokines is an inflammatory response that occurs in the early stages of atherosclerosis. Endothelial dysfunction in vascular inflammation begins with the expression of cell surface adhesion molecules by pro-inflammatory cytokines. The purpose of this study was to evaluate and verify the vascular inflammatory effects of isobavachalcone. In this study, we investigated the effects of isobavachalcone on inflammatory responses in vascular inflammation induced by the tumor necrosis factor-α (TNF-α) in human umbilical vein endothelial cells (HUVECs). TNF-α stimulation significantly increased the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) proteins, and concentration-dependently decreased by isobavachalcone in HUVECs. Isobavachalcone suppressed TNF-α-induced ICAM-1 and VCAM-1 expression in HUVECs, thereby inhibiting TNF-α-induced increase in monocyte adhesion. In addition, isobavachalcone decreased the phosphorylation of the NF-κB (necrosis factor κB) p65 subunit. The findings of this study demonstrate that isobavachalcone prevents TNF-α-induced vascular inflammation and has the potential to protect against the early progression of atherosclerosis.
中文翻译:
异巴伐查耳酮通过调节 NF-κB 信号通路减弱 TNF-α 诱导的人脐静脉内皮细胞 ICAM-1 和 VCAM-1 表达
由促炎细胞因子激活的血管炎症是发生在动脉粥样硬化早期阶段的炎症反应。血管炎症中的内皮功能障碍始于促炎细胞因子表达细胞表面粘附分子。本研究的目的是评估和验证异巴伐查酮的血管炎症作用。在这项研究中,我们研究了异巴伐查酮对人脐静脉内皮细胞 (HUVEC) 中由肿瘤坏死因子-α (TNF-α) 诱导的血管炎症反应的影响。TNF-α 刺激显着增加了细胞间粘附分子 1 (ICAM-1) 和血管细胞粘附分子 1 (VCAM-1) 蛋白的表达,并且异巴伐查酮在 HUVECs 中呈浓度依赖性降低。Isobavachalcone 抑制 TNF-α 诱导的 HUVECs 中 ICAM-1 和 VCAM-1 的表达,从而抑制 TNF-α 诱导的单核细胞粘附增加。此外,异巴伐查耳酮降低了 NF-κB(坏死因子 κB)p65 亚基的磷酸化。这项研究的结果表明,异巴伐查酮可预防 TNF-α 诱导的血管炎症,并有可能防止动脉粥样硬化的早期进展。
更新日期:2022-07-05
中文翻译:
异巴伐查耳酮通过调节 NF-κB 信号通路减弱 TNF-α 诱导的人脐静脉内皮细胞 ICAM-1 和 VCAM-1 表达
由促炎细胞因子激活的血管炎症是发生在动脉粥样硬化早期阶段的炎症反应。血管炎症中的内皮功能障碍始于促炎细胞因子表达细胞表面粘附分子。本研究的目的是评估和验证异巴伐查酮的血管炎症作用。在这项研究中,我们研究了异巴伐查酮对人脐静脉内皮细胞 (HUVEC) 中由肿瘤坏死因子-α (TNF-α) 诱导的血管炎症反应的影响。TNF-α 刺激显着增加了细胞间粘附分子 1 (ICAM-1) 和血管细胞粘附分子 1 (VCAM-1) 蛋白的表达,并且异巴伐查酮在 HUVECs 中呈浓度依赖性降低。Isobavachalcone 抑制 TNF-α 诱导的 HUVECs 中 ICAM-1 和 VCAM-1 的表达,从而抑制 TNF-α 诱导的单核细胞粘附增加。此外,异巴伐查耳酮降低了 NF-κB(坏死因子 κB)p65 亚基的磷酸化。这项研究的结果表明,异巴伐查酮可预防 TNF-α 诱导的血管炎症,并有可能防止动脉粥样硬化的早期进展。