IN VITRO MODULATION OF TNF-α AND CXCR4 PATHWAYS BY CANNABIS SATIVA–DERIVED CANNABIDIOL IN LPS/PMA/IL-1β–ACTIVATED THP-1
2. INTERNATIONAL MULTIDISCIPLINARY ENVIRONMENT AND HEMP CONGRESS, Bursa, Türkiye, 15 Aralık 2025, ss.31-38, (Tam Metin Bildiri)
- Yayın Türü: Bildiri / Tam Metin Bildiri
- Basıldığı Şehir: Bursa
- Basıldığı Ülke: Türkiye
- Sayfa Sayıları: ss.31-38
- Bursa Uludağ Üniversitesi Adresli: Evet
Özet
Cannabidiol (CBD), a major non-psychoactive phytocannabinoid of Cannabis sativa, has gained considerable attention as a natural immunomodulatory agent; however, its molecular effects under distinct inflammatory contexts remain insufficiently defined. This study investigated the immunomodulatory activity of C. sativa–derived CBD in vitro using the human monocytic THP-1 cell line. Inflammatory responses were induced through PMA differentiation followed by LPS- or IL-1β-mediated stimulation. After CBD administration (5 μg/mL), changes in TNF-α and CXCR4 gene expression were quantified by RT-qPCR. CBD markedly suppressed TNF-α expression in LPS/PMA-activated THP-1 cells (fold change: 0.36; p < 0.001) and significantly reduced CXCR4 levels, indicating a modulatory effect on both pro-inflammatory cytokine signaling and chemokine-mediated cell trafficking. In the IL1β model, CBD produced moderate but significant downregulation of both genes, suggesting a stimulation-dependent regulatory pattern. These findings reveal that CBD exerts conditionspecific immunomodulatory activity, with the strongest suppression observed in LPS-driven inflammatory pathways. Overall, the results demonstrate that C. sativa–derived CBD can modulate key inflammatory gene networks in human immune cells, supporting its potential as a natural candidate for the management of inflammatory and immune-mediated disorders. Future studies should explore broader cytokine panels, protein-level responses, and in vivo models to further elucidate CBD’s therapeutic relevance.
Keywords: Cannabidiol, Cannabis sativa, Immunomodulation, THP-1, TNF-α, CXCR4, LPS, IL-1β