Exploring the anti-inflammatory activity of sulforaphane.
Katie TreasureJames HarrisGary WilliamsonPublished in: Immunology and cell biology (2023)
Dysregulation of innate immune responses can result in chronic inflammatory conditions. Glucocorticoids, the current frontline therapy, are effective immunosuppressive drugs but come with a trade-off of cumulative and serious side effects. Therefore, alternative drug options with improved safety profiles are urgently needed. Sulforaphane, a phytochemical derived from plants of the brassica family, is a potent inducer of phase II detoxification enzymes via nuclear factor-erythroid factor 2-related factor 2 (NRF2) signaling. Moreover, a growing body of evidence suggests additional diverse anti-inflammatory properties of sulforaphane through interactions with mediators of key signaling pathways and inflammatory cytokines. Multiple studies support a role for sulforaphane as a negative regulator of nuclear factor kappa-light chain enhancer of activated B cells (NF-κB) activation and subsequent cytokine release, inflammasome activation and direct regulation of the activity of macrophage migration inhibitory factor. Significantly, studies have also highlighted potential steroid-sparing activity for sulforaphane, suggesting that it may have potential as an adjunctive therapy for some inflammatory conditions. This review discusses published research on sulforaphane, including proposed mechanisms of action, and poses questions for future studies that might help progress our understanding of the potential clinical applications of this intriguing molecule.
Keyphrases
- nuclear factor
- toll like receptor
- immune response
- phase ii
- anti inflammatory
- oxidative stress
- signaling pathway
- clinical trial
- case control
- transcription factor
- inflammatory response
- human health
- stem cells
- drug induced
- dendritic cells
- current status
- randomized controlled trial
- climate change
- systematic review
- minimally invasive
- risk assessment
- cell therapy
- lps induced
- pi k akt
- robot assisted
- induced apoptosis