New research published this week in the Journal of Cellular and Molecular Medicine[i] indicates that cannabidiol (CBD) protects the lungs of those infected with COVID-19 by boosting the concentration of a vital peptide. Known as apelin, the compound helps to regulate inflammation, blood pressure and immunity, and has been shown to become depleted in the lungs as a result of coronavirus.
While the anti-inflammatory properties of CBD and other cannabinoids are already fairly well documented, this latest finding represents a major step forward in our understanding of how these compounds produce this protective effect, and could have implications for the treatment of numerous respiratory and cardiovascular conditions.
COVID And Cannabinoids
The majority of people who suffer severe coronavirus symptoms develop a condition called Acute Respiratory Distress Syndrome (ARDS). As we reported in an earlier blog post, this is caused by the immune system going into overdrive and releasing a glut of inflammatory compounds called cytokines, resulting in a “cytokine storm” in the lungs.
Since the start of the pandemic, researchers have already discovered that THC treatment prevents this cytokine storm from occurring in mice with ARDS, leading to a 100 percent survival rate. On top of that, a new study was published last month indicating that CBD also downregulates the production of cytokines in the lungs of mice that had been infected with a virus that mimics the effects of COVID[ii].
While this is obviously excellent news, researchers had until now been unable to explain how these cannabinoids inhibit the release of cytokines in the presence of ARDS. Fortunately, the key now appears to have been found, with apelin being the magic ingredient.
What Is Apelin?
Apelin is produced in the lungs, heart, brain, fat tissue and blood, and is released in response to extreme changes in inflammation or blood pressure. For instance, when a lung infection occurs, apelin levels tend to go up in the surrounding cells in order to make sure that no cytokine storm occurs and everything continues to work as it should. In this way, it prevents ARDS from developing, or at the very least initiates a speedy recovery from ARDS.
In the new study, researchers infected mice with a COVID-like virus before measuring apelin levels in their lungs. Ordinarily, apelin concentrations would be expected to soar in response to such an infection, yet the study authors noted that the opposite occurred, as levels of the peptide plummeted to virtually zero.
This would seem to suggest that coronavirus somehow inhibits the production of apelin in the lungs, which would explain why it is so deadly.
However, after treating infected mice with CBD, apelin levels were restored. As a consequence, ARDS symptoms in these mice were reduced, while a closer examination revealed that the immune response of these rodents had been normalised along with oxygen flow and tissue damage in the lungs. In contrast, mice that had not received the cannabinoid saw no improvement in their condition.
All in all, these results suggest that CBD’s ability to stem the release of cytokines and reduce inflammation in the lungs is mediated by apelin, which for some reason is inhibited by coronavirus but restored following treatment with the cannabinoid.
Research is now ongoing to discover how this can be applied to humans suffering from COVID-19 and other ARDS-related conditions.
[i] Salles ÉL, Khodadadi H, Jarrahi A, Ahluwalia M, Paffaro Jr VA, Costigliola V, Yu JC, Hess DC, Dhandapani KM, Baban B. Cannabidiol (CBD) modulation of apelin in acute respiratory distress syndrome. Journal of Cellular and Molecular Medicine. – https://onlinelibrary.wiley.com/doi/10.1111/jcmm.15883
[ii] Khodadadi H, Salles ÉL, Jarrahi A, Chibane F, Costigliola V, Yu JC, Vaibhav K, Hess DC, Dhandapani KM, Baban B. Cannabidiol Modulates Cytokine Storm in Acute Respiratory Distress Syndrome Induced by Simulated Viral Infection Using Synthetic RNA. Cannabis and Cannabinoid Research. 2020 Sep 1;5(3):197-201. – https://www.liebertpub.com/doi/abs/10.1089/can.2020.0043
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