那么 COVID-19 和花生四烯酸途径呢？
What about COVID-19 and arachidonic acid pathway?
机构信息
Department of Chemical-Toxicological and Pharmacological Evaluations of Drugs, Faculty of Pharmacy, Catholic University Our Lady of Good Counsel, Rruga Dritan Hoxha, Tirana, Albania.
出版信息
Eur J Clin Pharmacol. 2020 Nov;76(11):1501-1504. doi: 10.1007/s00228-020-02941-w. Epub 2020 Jun 25.
BACKGROUND AND OBJECTIVE
COVID-19 is a highly contagious viral disease. In this study, we tried to define and discuss all the findings on the potential association between arachidonic acid (AA) pathway and COVID-19 pathophysiology.
METHODS
A literature search across PubMed, Scopus, Embase, and Cochrane database was conducted. A total of 25 studies were identified.
RESULTS
The data elucidated that COX-2 and prostaglandins (PGs), particularly PGE, have pro-inflammatory action in COVID-19 pathophysiology. Arachidonic acid can act as endogenous antiviral compound. A deficiency in AA can make humans more susceptible to COVID-19. Targeting these pro-inflammatory mediators may help in decreasing the mortality and morbidity rate in COVID-19 patients.
CONCLUSIONS
PGE levels and other PGs levels should be measured in patients with COVID-19. Lowering the PGE levels through inhibition of human microsomal prostaglandin E synthase-1 (mPGES-1) can enhance the host immune response against COVID-19. In addition, the hybrid compounds, such as COX-2 inhibitors/TP antagonists, can be an innovative treatment to control the overall balance between AA mediators in patients with COVID-19.
背景与目的
COVID-19 是一种高度传染性的病毒性疾病。在本研究中，我们试图定义并讨论花生四烯酸（AA）途径与 COVID-19 病理生理学之间潜在关联的所有发现。
方法
在 PubMed、Scopus、Embase 和 Cochrane 数据库中进行了文献检索。共确定了 25 项研究。
结果
数据表明，COX-2 和前列腺素（PGs），特别是 PGE，在 COVID-19 病理生理学中具有促炎作用。花生四烯酸可以作为内源性抗病毒化合物。AA 缺乏会使人类更容易感染 COVID-19。靶向这些促炎介质可能有助于降低 COVID-19 患者的死亡率和发病率。
结论
应在 COVID-19 患者中测量 PGE 水平和其他 PG 水平。通过抑制人微粒体前列腺素 E 合酶-1（mPGES-1）降低 PGE 水平可以增强宿主对 COVID-19 的免疫反应。此外，如 COX-2 抑制剂/TP 拮抗剂等混合化合物可能是控制 COVID-19 患者 AA 介质整体平衡的创新治疗方法。
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