期刊
PEERJ
卷 9, 期 -, 页码 -出版社
PEERJ INC
DOI: 10.7717/peerj.12262
关键词
Cannabinoids; SARS-Cov-2; COVID-19; Human iPSC-derived cardiomyocytes; WIN 55,212-2
资金
- National Council of Scientific and Technological Development (CNPq) [313688/2020-6]
- Coordination for the Improvement of Higher Education Personnel (CAPES)
- CNPq
- D'Or Institute for Research and Education (IDOR)
The study suggests that cannabinoids can alleviate myocardial injury in COVID-19 patients by suppressing inflammation, reducing levels of cytokines, and attenuating cytotoxic damage.
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can infect several organs, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 is myocardial injury, which is associated with a high risk of mortality. Myocardial injury, caused directly or indirectly by SARS-CoV-2 infection, can be triggered by inflammatory processes that lead to damage to the heart tissue. Since one of the hallmarks of severe COVID-19 is the cytokine storm, strategies to control inflammation caused by SARS-CoV-2 infection have been considered. Cannabinoids are known to have anti-inflammatory properties by negatively modulating the release of pro-inflammatory cytokines. Herein, we investigated the effects of the cannabinoid agonist WIN 55,212-2 (WIN) in human iPSC-derived cardiomyocytes (hiPSC-CMs) infected with SARS-CoV-2. WIN did not modify angiotensin-converting enzyme II protein levels, nor reduced viral infection and replication in hiPSC-CMs. On the other hand, WIN reduced the levels of interleukins six, eight, 18 and tumor necrosis factor-alpha (TNF-alpha) released by infected cells, and attenuated cytotoxic damage measured by the release of lactate dehydrogenase (LDH). Our findings suggest that cannabinoids should be further explored as a complementary therapeutic tool for reducing inflammation in COVID-19 patients.
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