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D-柠檬烯是一种潜在的单萜类化合物，可抑制2019冠状病毒病肺纤维化中的PI3K/Akt/IKK-α/NF-κB p65信号通路。

D-Limonene Is a Potential Monoterpene to Inhibit PI3K/Akt/IKK-α/NF-κB p65 Signaling Pathway in Coronavirus Disease 2019 Pulmonary Fibrosis.

作者信息

Yang Fan, Chen Ru, Li Wan-Yang, Zhu Hao-Yue, Chen Xiao-Xuan, Hou Zhen-Feng, Cao Ren-Shuang, Zang GuoDong, Li Yu-Xuan, Zhang Wei

机构信息

College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

Biomedical Research Institute of Fudan University, Shanghai, China.

出版信息

Front Med (Lausanne). 2021 Mar 9;8:591830. doi: 10.3389/fmed.2021.591830. eCollection 2021.

DOI:10.3389/fmed.2021.591830
PMID:33768100
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7985179/
Abstract

At the time of the prevalence of coronavirus disease 2019 (COVID-19), pulmonary fibrosis (PF) related to COVID-19 has become the main sequela. However, the mechanism of PF related to COVID (COVID-PF) is unknown. This study aimed to explore the key targets in the development of COVID-PF and the mechanism of d-limonene in the COVID-PF treatment. The differentially expressed genes of COVID-PF were downloaded from the GeneCards database, and their pathways were analyzed. d-Limonene was molecularly docked with related proteins to screen its pharmacological targets, and a rat lung fibrosis model was established to verify d-limonene's effect on COVID-PF-related targets. The results showed that the imbalance between collagen breakdown and metabolism, inflammatory response, and angiogenesis are the core processes of COVID-PF; and PI3K/AKT signaling pathways are the key targets of the treatment of COVID-PF. The ability of d-limonene to protect against PF induced by bleomycin in rats was reported. The mechanism is related to the binding of PI3K and NF-κB p65, and the inhibition of PI3K/Akt/IKK-α/NF-κB p65 signaling pathway expression and phosphorylation. These results confirmed the relationship between the PI3K-Akt signaling pathway and COVID-PF, showing that d-limonene has a potential therapeutic value for COVID-PF.

摘要

在2019冠状病毒病（COVID-19）流行期间，与COVID-19相关的肺纤维化（PF）已成为主要后遗症。然而，与COVID相关的PF（COVID-PF）的发病机制尚不清楚。本研究旨在探索COVID-PF发展过程中的关键靶点以及d-柠檬烯在COVID-PF治疗中的作用机制。从GeneCards数据库下载COVID-PF的差异表达基因，并对其通路进行分析。将d-柠檬烯与相关蛋白进行分子对接以筛选其药理靶点，并建立大鼠肺纤维化模型以验证d-柠檬烯对COVID-PF相关靶点的作用。结果表明，胶原蛋白分解与代谢失衡、炎症反应和血管生成是COVID-PF的核心过程；PI3K/AKT信号通路是治疗COVID-PF的关键靶点。已有报道称d-柠檬烯具有保护大鼠免受博莱霉素诱导的PF的能力。其机制与PI3K和NF-κB p65的结合以及PI3K/Akt/IKK-α/NF-κB p65信号通路表达和磷酸化的抑制有关。这些结果证实了PI3K-Akt信号通路与COVID-PF之间的关系，表明d-柠檬烯对COVID-PF具有潜在的治疗价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/4d60e9a32972/fmed-08-591830-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/18a6477cde38/fmed-08-591830-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/ec035b12251d/fmed-08-591830-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/a94d3a8f47e0/fmed-08-591830-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/4d60e9a32972/fmed-08-591830-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/18a6477cde38/fmed-08-591830-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/81c4d260fc52/fmed-08-591830-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/c5c15252f4c7/fmed-08-591830-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/c56bd9862f3e/fmed-08-591830-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/ec035b12251d/fmed-08-591830-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/a94d3a8f47e0/fmed-08-591830-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a81/7985179/4d60e9a32972/fmed-08-591830-g0007.jpg

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