图德卡通过调节ER压力信号通路和抑制自来抑制EV71复制
Siwen Wang1, Rui Liu1, Yuting Zhou2
1Molecular Diagnostic Laboratory, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210003, PR China; Children's Health Center, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210003, PR China; The Second Clinical College of Nanjing Medical University, Nanjing, Jiangsu 210011, PR China.
Diagnostic microbiology and infectious disease
|August 30, 2024
概括
陶氏氧醇酸 (TUDCA) 有效地抑制了肠道病毒71 (EV71) 在细胞中的复制. 这种胆汁酸通过调节未折叠蛋白反应 (UPR) 和抑制自而起作用,提供了潜在的治疗策略.
科学领域:
- 细胞生物学 细胞生物学
- 病毒学 病毒学
- 生物化学 生物化学
背景情况:
- 众所周知,肠道病毒71 (EV71) 感染会操纵细胞内质网膜 (ER) 应激和自途径,以促进病毒复制.
- 塔乌尔苏氧化胆酸 (TUDCA) 是一种含水性胆酸,具有减轻ER压力和预防亡的证明性质.
研究的目的:
- 研究TUDCA预处理对人类细胞系EV71复制的作用.
- 阐明TUDCA影响EV71感染的潜在机制,特别是关于ER压力和自.
主要方法:
- 在感染EV71之前,HeLa和Vero细胞经过不同度的TUDCA预处理.
- 分析了关键未折叠蛋白反应 (UPR) 传感器蛋白 (ATF6,PERK,IRE1) 的表达水平.
- 在TUDCA治疗的和受感染的细胞中评估了自水平.
主要成果:
- 在TUDCA前期治疗中,在HeLa和Vero细胞中显示出EV71复制的剂量依赖性抑制.
- 图德卡通过对ATF6进行上调和对PERK和IRE1进行下调调节了UPR.
- 该研究观察到TUDCA治疗的细胞中抑制了自,这是UPR的下游过程.
结论:
- 通过干扰病毒复制,TUDCA对EV71表现出抗病毒特性.
- 该机制涉及UPR传感器蛋白的调节和随后的自抑制.
- 通过准细胞应激通路,TUDCA代表了对EV71感染的潜在治疗剂.
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