The Potential Anti-Inflammatory Effect of Cannabidiol in Autoimmune Myocarditis

Background: Myocarditis is an inflammatory heart disease that can be life-threatening, especially for young adults and adolescents. Acute myocarditis can be caused by viral infections that lead to inflammation, tissue damage, and ultimately heart failure. The virus triggers an autoimmune reaction, with cardiac myosin being an important autoantigen. However, conventional immunosuppressive therapy, often used to treat autoimmune myocarditis, can have toxic effects, causing poor outcomes. In addition, few clinical trials on the treatment of myocarditis have resulted in a limited choice of therapeutic strategies, underscoring the need for new options. Cannabidiol (CBD), a nonpsychoactive phytocannabinoid, has clinically proven immunosuppressive effects, including anti-inflammatory, antioxidant, and cytoprotective properties. The use of CBD has been approved by the FDA for the treatment of refractory epilepsy in children and glioblastoma multiforme. In this study, we propose an experimental model of autoimmune myocarditis to investigate the anti-inflammatory effects of CBD on immune cell-mediated inflammation triggered by cardiac myosin.

Methods: A co-culture of human differentiated THP-1 macrophages and Jurkat CD4+ T-cells was pretreated with CBD for 1 hour, followed by stimulation with α-MyHC for 4 hours. Gene expressions of inflammatory cytokines (IL-1b, IL-6, IL-2, IL-4, IL-18, IL-10, TNF-a, IFN-γ), CCL2 (MCP-1), and mediators for vascular permeability (VEGF-A, ICAM) were investigated via RT-qPCR.

Results: We observed that CBD significantly attenuated α-MyHC-induced expressions of the inflammatory cytokines IL-1b, IL-6, IL-4, as well as the CC chemokine MCP-1 in a dose-dependent manner. In contrast, a high concentration of CBD (20 mM) induced a significant increase in IL-2 and IL-18, as well as VEGF-A and ICAM expression relative to α-MyHC-treated and experimental control. No significant differences were observed in IL-10, TNF-a, or IFN-γ expression relative to α-MyHC-treated and experimental control.

Conclusion: Our findings show CBD exerts a dual, dose-dependent effect on α-MyHC-stimulated immune cells. Lower concentrations of CBD suppress pro-inflammatory cytokines and chemokines expressions, while higher concentrations upregulate IL-2, IL-18, VEGF-A, and ICAM, indicating a shift toward immune activation and vascular permeability. These findings highlight CBD’s therapeutic potential in autoimmune myocarditis, while underscoring the importance of precise dosing. Therefore, further studies to elucidate the mechanisms underlying these dose-dependent effects and their relevance in vivo are warranted.

No conflict of interest has been declared by the author(s).

Publication History

Article published online:
17 February 2026