TUDCA 通过调节 ER 应激信号通路和抑制自噬来抑制 EV71 复制

IF 2.1 4区 医学 Q3 INFECTIOUS DISEASES
Siwen Wang , Rui Liu , Yuting Zhou , Jinjin Xu , Airong Su , Datong Zheng
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引用次数: 0

摘要

牛磺脱氧胆酸(TUDCA)是一种天然亲水性胆汁酸,可减轻内质网(ER)应激和抑制细胞凋亡,从而保护细胞。以前的研究表明,肠道病毒 71(EV71)感染会调节 ER 应激,诱导自噬以帮助病毒复制。本研究观察了 TUDCA 预处理对感染 EV71 的 HeLa 和 Vero 细胞的影响,发现 TUDCA 可抑制 EV71 在 TUDCA 预处理过的 HeLa 和 Vero 细胞中的复制,且呈剂量依赖性。我们发现,TUDCA预处理通过调节UPR的三个分支(即上调ATF6、下调PERK和IRE1)来抑制EV71的复制。结果还表明,作为 UPR 下游的自噬也受到了抑制。结果表明,TUDCA 在ER应激后通过调节UPR传感器蛋白和自噬抑制了EV71的复制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TUDCA inhibits EV71 replication by regulating ER stress signaling pathway and suppressing autophagy

Tauroursodeoxycholic acid (TUDCA) is a naturally occurring hydrophilic bile acid that alleviates endoplasmic reticulum (ER) stress and inhibits apoptosis, thereby protecting cells. Previous studies have shown that enterovirus 71 (EV71) infection modulates ER stress and induces autophagy to assist viral replication. This study observed the effects of TUDCA pretreatment on HeLa and Vero cells infected with EV71, finding that TUDCA inhibits EV71 replication in TUDCA pretreated HeLa and Vero cells in a dose-dependent manner. We found that TUDCA pretreatment inhibited EV71 replication by regulating three branches of UPR, that is up-regulated ATF6, down-regulated both PERK and IRE1. The results also indicated that autophagy which is downstream of UPR, was inhibited either. The results indicate that TUDCA inhibits EV71 replication by regulating UPR sensor proteins and autophagy following ER stress.

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来源期刊
CiteScore
5.30
自引率
3.40%
发文量
149
审稿时长
56 days
期刊介绍: Diagnostic Microbiology and Infectious Disease keeps you informed of the latest developments in clinical microbiology and the diagnosis and treatment of infectious diseases. Packed with rigorously peer-reviewed articles and studies in bacteriology, immunology, immunoserology, infectious diseases, mycology, parasitology, and virology, the journal examines new procedures, unusual cases, controversial issues, and important new literature. Diagnostic Microbiology and Infectious Disease distinguished independent editorial board, consisting of experts from many medical specialties, ensures you extensive and authoritative coverage.
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