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靶向 COVID-19 治疗性 NRICM102 诱导的刺突蛋白 TLR/NET 轴可改善肺栓塞和纤维化。

Targeting spike protein-induced TLR/NET axis by COVID-19 therapeutic NRICM102 ameliorates pulmonary embolism and fibrosis.

机构信息

National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 112026, Taiwan.

National Research Institute of Chinese Medicine, Ministry of Health and Welfare, Taipei 112026, Taiwan; Department of Biochemical Science and Technology, National Chiayi University, Chiayi 600355, Taiwan.

出版信息

Pharmacol Res. 2022 Oct;184:106424. doi: 10.1016/j.phrs.2022.106424. Epub 2022 Sep 5.

DOI:10.1016/j.phrs.2022.106424
PMID:36064077
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9443660/
Abstract

The global COVID-19 pandemic remains a critical public health threat, as existing vaccines and drugs appear insufficient to halt the rapid transmission. During an outbreak from May to August 2021 in Taiwan, patients with severe COVID-19 were administered NRICM102, which was a traditional Chinese medicine (TCM) formula developed based on its predecessor NRICM101 approved for treating mild cases. This study aimed to explore the mechanism of NRICM102 in ameliorating severe COVID-19-related embolic and fibrotic pulmonary injury. NRICM102 was found to disrupt spike protein/ACE2 interaction, 3CL protease activity, reduce activation of neutrophils, monocytes and expression of cytokines (TNF-α, IL-1β, IL-6, IL-8), chemokines (MCP-1, MIP-1, RANTES) and proinflammatory receptor (TLR4). NRICM102 also inhibited the spread of virus and progression to embolic and fibrotic pulmonary injury through reducing prothrombotic (vWF, PAI-1, NET) and fibrotic (c-Kit, SCF) factors, and reducing alveolar type I (AT1) and type II (AT2) cell apoptosis. NRICM102 may exhibit its protective capability via regulation of TLRs, JAK/STAT, PI3K/AKT, and NET signaling pathways. The study demonstrates the ability of NRICM102 to ameliorate severe COVID-19-related embolic and fibrotic pulmonary injury in vitro and in vivo and elucidates the underlying mechanisms.

摘要

全球 COVID-19 大流行仍然是一个严重的公共卫生威胁，因为现有的疫苗和药物似乎不足以阻止其快速传播。在 2021 年 5 月至 8 月台湾爆发的疫情中，严重 COVID-19 患者使用了 NRICM102，这是一种基于其前身 NRICM101 开发的中药（TCM）配方，用于治疗轻症。本研究旨在探讨 NRICM102 改善严重 COVID-19 相关栓塞和纤维化性肺损伤的机制。NRICM102 被发现可破坏刺突蛋白/ACE2 相互作用、3CL 蛋白酶活性，减少中性粒细胞、单核细胞的激活以及细胞因子（TNF-α、IL-1β、IL-6、IL-8）、趋化因子（MCP-1、MIP-1、RANTES）和促炎受体（TLR4）的表达。NRICM102 还通过减少促血栓形成（vWF、PAI-1、NET）和纤维化（c-Kit、SCF）因子，以及减少肺泡 I 型（AT1）和 II 型（AT2）细胞凋亡，抑制病毒传播和进展为栓塞和纤维化性肺损伤。NRICM102 可能通过调节 TLRs、JAK/STAT、PI3K/AKT 和 NET 信号通路发挥其保护作用。该研究证明了 NRICM102 在体外和体内改善严重 COVID-19 相关栓塞和纤维化性肺损伤的能力，并阐明了其潜在机制。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c1b/9443660/c5f367d723f6/gr5a_lrg.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c1b/9443660/6885094fcdc1/gr8_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c1b/9443660/15052f328d69/gr9_lrg.jpg
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