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多粘菌素B通过靶向内体分选转运复合体Ⅲ(ESCRT-III)机制和RIPK1/RIPK3/混合谱系激酶结构域样蛋白(MLKL)信号通路减轻缺血性脑卒中大鼠的脑损伤。

Polymyxin B Reduces Brain Injury in Ischemic Stroke Rat Through a Mechanism Involving Targeting ESCRT-III Machinery and RIPK1/RIPK3/MLKL Pathway.

作者信息

Tian Jing, Zhang Yi-Yue, Peng Ya-Wei, Liu Bin, Zhang Xiao-Jie, Hu Zhong-Yang, Hu Chang-Ping, Luo Xiu-Ju, Peng Jun

机构信息

Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, 410078, China.

Hunan Provincial Key Laboratory of Cardiovascular Research, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, 410078, China.

出版信息

J Cardiovasc Transl Res. 2022 Oct;15(5):1129-1142. doi: 10.1007/s12265-022-10224-1. Epub 2022 Mar 3.

Abstract

Endosomal sorting complex required for transport III (ESCRT-III) machinery is a key component to counteract the mixed lineage kinase domain-like pseudokinase (MLKL)-induced plasma membrane broken in cells undergoing necroptosis. Based on the bioinformatics analysis, polymyxin B, a polypeptide antibiotic, is predicted to simultaneously interact with ESCRT-III subunits and necroptosis-relevant proteins. This study aims to explore whether polymyxin B could reduce necroptosis in the stroke rat brain via enhancing the ESCRT-III machinery and/or suppressing the RIPK1/RIPK3/MLKL pathway. The stroke rats showed evident brain injury, concomitant with the downregulation of ESCRT-III subunits and the upregulation of necroptosis-relevant proteins. Post-ischemic administration of polymyxin B could alleviate the brain injury, accompanied by restoration of the levels of ESCRT-III subunits and suppression of necroptosis-relevant proteins. And, polymyxin B exerted similar effects in hypoxia-treated HT22 cells. We conclude that polymyxin B can reduce necroptosis in the stroke rat brain via enhancing the ESCRT-III machinery and suppressing the RIPK1/RIPK3/MLKL pathway simultaneously.

摘要

转运所需内体分选复合物III(ESCRT-III)机制是在经历坏死性凋亡的细胞中对抗混合谱系激酶结构域样假激酶(MLKL)诱导的质膜破裂的关键组成部分。基于生物信息学分析,多粘菌素B(一种多肽抗生素)预计会同时与ESCRT-III亚基和坏死性凋亡相关蛋白相互作用。本研究旨在探讨多粘菌素B是否可通过增强ESCRT-III机制和/或抑制RIPK1/RIPK3/MLKL途径来减少中风大鼠脑内的坏死性凋亡。中风大鼠表现出明显的脑损伤,同时伴有ESCRT-III亚基下调和坏死性凋亡相关蛋白上调。缺血后给予多粘菌素B可减轻脑损伤,同时伴有ESCRT-III亚基水平恢复和坏死性凋亡相关蛋白受抑制。并且,多粘菌素B在缺氧处理的HT22细胞中也发挥了类似作用。我们得出结论,多粘菌素B可通过同时增强ESCRT-III机制和抑制RIPK1/RIPK3/MLKL途径来减少中风大鼠脑内的坏死性凋亡。

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