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硒二唑通过氧化损伤介导的Bcl-2/Stat 3/NF-κB信号通路抑制腺病毒诱导的细胞凋亡。

Selenadiazole Inhibited Adenovirus-Induced Apoptosis through the Oxidative-Damage-Mediated Bcl-2/Stat 3/NF-κB Signaling Pathway.

作者信息

Liu Xia, Lai Jia, Su Jingyao, Zhang Kelan, Li Jiali, Li Chuqing, Ning Zhihui, Wang Chenyang, Zhu Bing, Li Yinghua, Zhao Mingqi

机构信息

Center Laboratory, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.

出版信息

Pharmaceuticals (Basel). 2023 Oct 16;16(10):1474. doi: 10.3390/ph16101474.

DOI:10.3390/ph16101474
PMID:37895944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10610542/
Abstract

Human adenovirus type 7 (HAdV7) infection causes severe pneumonia, yet there are still no breakthroughs in treatment options for adenovirus, and the road to antiviral drug development faces major challenges. We attempted to find new drugs and we stumbled upon one: selenadiazole. Selenadiazole has been shown to have significant anti-tumor effects due to its unique chemical structure and drug activity. However, its effectiveness against viruses has not been evaluated yet. In our study, selenadiazole also showed superior antiviral activity. In vitro experiments, selenadiazole was able to inhibit adenovirus-mediated mitochondrial-oxidative-damage-related apoptosis, and in in vivo experiments, selenadiazole was able to inhibit apoptosis by modulating the apoptotic signaling pathway Bcl-2/Stat3/NF-κB, etc., and was able to largely attenuate adenovirus-infection-induced pneumonia and lung injury in mice. This study aims to describe a new antiviral treatment option from the perspective of anti-adenovirus-mediated oxidative stress and its associated apoptosis and to provide theoretical guidance for the treatment of clinical adenovirus infection to a certain extent.

摘要

人7型腺病毒(HAdV7)感染可导致严重肺炎,但腺病毒的治疗选择仍未取得突破,抗病毒药物研发之路面临重大挑战。我们试图寻找新药,偶然发现了一种:硒二唑。由于其独特的化学结构和药物活性,硒二唑已显示出显著的抗肿瘤作用。然而,其对病毒的有效性尚未得到评估。在我们的研究中,硒二唑也显示出卓越的抗病毒活性。在体外实验中,硒二唑能够抑制腺病毒介导的与线粒体氧化损伤相关的细胞凋亡,在体内实验中,硒二唑能够通过调节凋亡信号通路Bcl-2/Stat3/NF-κB等抑制细胞凋亡,并能够在很大程度上减轻腺病毒感染诱导的小鼠肺炎和肺损伤。本研究旨在从抗腺病毒介导的氧化应激及其相关细胞凋亡的角度描述一种新的抗病毒治疗选择,并在一定程度上为临床腺病毒感染的治疗提供理论指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d8/10610542/223d538f0c57/pharmaceuticals-16-01474-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d8/10610542/223d538f0c57/pharmaceuticals-16-01474-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d8/10610542/b72f9948496b/pharmaceuticals-16-01474-g002.jpg
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