摘要
目的探讨在LPS引起的炎症状态下A20对人脐静脉内皮细胞凋亡、成管的影响及可能机制。方法获取人脐带静脉内皮细胞,转染A20慢病毒后LPS刺激下利用CCK-8及流式细胞术检测内皮细胞凋亡情况,显微镜下观测成管实验;Western blotting检测NF-κB通路活化情况;ELISA法检测培养上清中可溶性E-selectin的分泌情况。结果 1)与正常对照相比,A20抑制炎症刺激下人脐静脉内皮细胞的凋亡率(P<0.001);2)与正常对照相比,A20促进炎症刺激下人脐静脉内皮细胞成管率(P<0.001);3)在炎症状态下A20通过抑制NF-κB通路对人脐静脉内皮细胞起保护作用。结论 LPS引起的炎症状态下,A20可通过抑制NF-κB通路使E-selectin表达降低,从而保护炎症状态下的人脐静脉内皮细胞活性及功能,提示A20可作为干预心脑血管患者血管内皮细胞的一个重要靶点。
To investigate the effect of A20 on human umbilical vein endothelial cell （HUVEC） under LPS-induced inflammatory state and its underlying mechanisms, the apoptosis of HUVEC after LPS stimulation was detected by CCK-8 and flow cytometry methods, and the tube forming experiment was observed under the microscope. The activation of NF- kappa B pathway and the secretion of soluble E-seleetin in supematant were detected by Western blotting and ELISA, respectively. Data showed that A20 inhibited the apoptosis rate of LPS-stimulated HUVEC （P〈0.001）, as compared to control. Moreover, A20 promoted the rate of tube forming of LPS-stimulated HUVEC （P〈0.001）, and protected the HUVEC from inflammation by inhibiting the NF-kappa B pathway. In conclusion, A20 can reduce E-selectin expression by inhibiting NF-kappa B pathway under the condition of LPS-induced inflammation, thus protects the HUVEC activity and function from inflammatory stimulation, suggesting A20 can be considered as a biomarker and target in cardiovascular diseases treatment.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2018年第2期115-119,共5页
Immunological Journal
关键词
A20
炎症
NF-ΚB
人脐静脉内皮细胞
A20
Inflammation
NF-kappa B
Human umbilical vein endothelial cell
