TIR/BB-loop mimetic AS-1 protects vascular endothelial cells from injury induced by hypoxia/reoxygen

• 作 者: Zhijia Zhang Yuxing Hou Jiantao Li Chao Tang Linli Que Qian Tan Yuehua Li
• 机 构: Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China;Department
• 出 处: 生物医学研究杂志（英文版）
• 发表日期: 2020年5期
• 关键词: AS-1 vascular endothelial cells hypoxia/reoxygenation IL-1R NF-κB MAPK

Morphological and functional abnormalities of vascular endothelial cells (VECs) are risk factors of ischemiareperfusion in skin flaps.Signaling pathway mediated by interleukin-1 receptor (IL-1R) is essential to hypoxia/reoxygenation (H/R) injury of VECs.While the TIR/BB-loop mimetic (AS-1) disrupts the interaction between IL-1R and myeloid differentiation primary-response protein 88 (MyD88),its role in the VECs dysfunction under H/R is unclear.In this study,we first showed that there was an infiltration of inflammatory cells and the apoptosis of VECs by using a skin flap section from patients who received flap transplantation.We then showed that the H/R treatment induced apoptosis and loss of cell migration of endothelial cell line H926 were attenuated by AS-1.Furthermore,our data suggested that AS-1 inhibits the interaction between IL-1R and MyD88,and subsequent phosphorylation of IκB and p38 pathway,as well as the nuclear localization of NF-KB subunit p65/p50.Thus,this study indicated that the protective role of AS-1 in H/R induced cellular injury may be due to the AS-1 mediated down-regulation of IL-1R signaling pathway.