Abstract
Cannabidiol (CBD), a non-psychoactive compound from Cannabis sativa, shows promise as a therapeutic agent for conditions associated with inflammation and oxidative stress, often involving nitric oxide (NO) signaling dysregulation. This review summarizes preclinical and clinical data on CBD’s impact on nitric oxide synthase (NOS) isoforms and NO levels in cardiovascular, neurological, metabolic, and immune systems. Studies suggest that CBD can reduce inflammation-induced inducible NOS (iNOS) expression while maintaining or enhancing endothelial NOS (eNOS)-mediated NO production, leading to decreased oxidative stress, improved endothelial function, and reduced neuroinflammation. The effects of CBD vary based on dose, formulation, timing, and disease state, with potential interactions with metabolites and other drugs affecting safety. Further research is needed to determine optimal dosing, formulation, pharmacokinetics, metabolite profiles, and long-term safety for specific conditions.