Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway

Cannabinoid compounds have potential as treatments for a variety of conditions, with cannabigerol (CBG) being known for its anti-inflammatory properties. In this study, we investigated the effects of CBG in a cellular model of 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD). In the cellular model, we confirmed the cytotoxicity of CBG and downregulated the expression of inflammatory markers <i>CCL26</i>, <i>IL1B</i>, <i>IL6</i>, and <i>TNF</i> (<i>p</i> < 0.001). In the mouse model, clinical, histological, and immunological changes were analyzed. The results showed that CBG improved dermatitis severity score, epidermal thickness, and mast cell count and reduced inflammatory cytokines (<i>Tslp</i>, <i>Il1b</i>, <i>Il4</i>, <i>Il6</i>, <i>Il13</i>, <i>Il17</i>, <i>Il18</i>, <i>Il22</i>, and <i>Il33</i>) by qRT-PCR (<i>p</i> < 0.001). Western blot results showed modulated changes in JAK1, JAK2, TYK2, STAT1, STAT2, STAT3, p-STAT3, STAT6, and p-STAT6 (<i>p</i> < 0.05). Subsequently, p-IκBα, NF-κB, and p-NF-κB signaling factors were also reduced (<i>p</i> < 0.05), with corresponding changes in skin barrier factors. The results of this study indicate that CBG effectively alleviates AD-like symptoms and suggest the potential of CBG as a therapeutic agent.