TIR/BB-loop mimetic AS-1 protects vascular endothelial cells from injury induced by hypoxia/reoxygenation
Zhijia Zhang1
Yuxing Hou2
Jiantao Li2
Chao Tang2
Linli Que2
Qian Tan3
Yuehua Li2
1.Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China;Department of Plasticsurgery, Drum Tower Hospital, Nanjing, Jiangsu 211100, China2.Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 211166, China3.Department of Plasticsurgery, Drum Tower Hospital, Nanjing, Jiangsu 211100, China
摘要：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.
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分类号：R622(整形外科学（修复外科学）)
论文发表日期：2020-09-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：8( 343-350 )
英文信息