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双氢青蒿素通过抑制 JAK2/STAT3 信号通路减轻大鼠肺部炎症和纤维化。

Dihydroartemisinin attenuates pulmonary inflammation and fibrosis in rats by suppressing JAK2/STAT3 signaling.

机构信息

Department of Gastrointestinal Surgery, Taizhou Clinical Medical School of Nanjing Medical University (Taizhou People's Hospital), Taizhou 225300, Jiangsu, China.

Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, Jiangsu, China.

出版信息

Aging (Albany NY). 2022 Feb 4;14(3):1110-1127. doi: 10.18632/aging.203874.

DOI:10.18632/aging.203874
PMID:35120332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8876897/
Abstract

Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has induced a worldwide pandemic since early 2020. COVID-19 causes pulmonary inflammation, secondary pulmonary fibrosis (PF); however, there are still no effective treatments for PF. The present study aimed to explore the inhibitory effect of dihydroartemisinin (DHA) on pulmonary inflammation and PF, and its molecular mechanism. Morphological changes and collagen deposition were analyzed using hematoxylin-eosin staining, Masson staining, and the hydroxyproline content. DHA attenuated early alveolar inflammation and later PF in a bleomycin-induced rat PF model, and inhibited the expression of interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNFα), and chemokine (C-C Motif) Ligand 3 (CCL3) in model rat serum. Further molecular analysis revealed that both pulmonary inflammation and PF were associated with increased transforming growth factor-β1 (TGF-β1), Janus activated kinase 2 (JAK2), and signal transducer and activator 3(STAT3) expression in the lung tissues of model rats. DHA reduced the inflammatory response and PF in the lungs by suppressing TGF-β1, JAK2, phosphorylated (p)-JAK2, STAT3, and p-STAT3. Thus, DHA exerts therapeutic effects against bleomycin-induced pulmonary inflammation and PF by inhibiting JAK2-STAT3 activation. DHA inhibits alveolar inflammation, and attenuates lung injury and fibrosis, possibly representing a therapeutic candidate to treat PF associated with COVID-19.

摘要

新型冠状病毒病（COVID-19）由 SARS-CoV-2 引起，自 2020 年初以来引发了全球大流行。COVID-19 引起肺部炎症，继发肺纤维化（PF）；然而，目前仍然没有针对 PF 的有效治疗方法。本研究旨在探讨双氢青蒿素（DHA）对肺部炎症和 PF 的抑制作用及其分子机制。通过苏木精-伊红染色、马松染色和羟脯氨酸含量分析形态变化和胶原沉积。DHA 减轻博莱霉素诱导的大鼠 PF 模型中的早期肺泡炎症和后期 PF，并抑制模型大鼠血清中白细胞介素（IL）-1β、IL-6、肿瘤坏死因子 α（TNFα）和趋化因子（C-C 基序）配体 3（CCL3）的表达。进一步的分子分析表明，肺部炎症和 PF 均与模型大鼠肺组织中转化生长因子-β1（TGF-β1）、Janus 激活激酶 2（JAK2）和信号转导和转录激活因子 3（STAT3）表达增加有关。DHA 通过抑制 TGF-β1、JAK2、磷酸化（p）-JAK2、STAT3 和 p-STAT3 减轻肺部炎症反应和 PF。因此，DHA 通过抑制 JAK2-STAT3 激活对博莱霉素诱导的肺部炎症和 PF 发挥治疗作用。DHA 抑制肺泡炎症，减轻肺损伤和纤维化，可能是治疗 COVID-19 相关 PF 的治疗候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1088/8876897/ad8ce1050008/aging-14-203874-g008.jpg
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