Anti-inflammatory effects of cannabidiol in the treatment of type 1 diabetes: A mini review

Figure 4 High glucose levels increase mitochondrial activity, leading to the production of reactive oxygen species, which activates the nuclear factor kappa B/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 inflammasome pathway. This activation raises pro-inflammatory cytokines [tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β)], promoting CD4+ and CD8+ T-cell activation and resulting in β-cell death. Cannabidiol (CBD) inhibits nuclear factor kappa B (NF-κB)/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) activation, thereby reducing TNF-α and IL-1β levels. This downregulates CD4+ and CD8+ T-cell activity, contributing to β-cell survival.