Table 1.
Summary of sulforaphane biological activities.
| Bioactivity | Mechanism | Reference |
|---|---|---|
| Anti-inflammatory | ↓proinflammatory markers, ↓NF- kB | (20–23) |
| Anticancer | ↑cell cycle arrest, ↓metastases, ↓angiogenesis ↑apoptosis, ↑Nrf2 |
(24–26) |
| Protects the DNA, ↑ histone deacetylase | (27–30) | |
| ↑Nrf2 antioxidant signaling cascade | (29, 31–34) | |
| Antioxidant | ↑antioxidant defense, ↑GSH | (22, 35, 36) |
| Cardioprotective | ↓oxidative stress ↑TRxRS, ↑GR, ↑GSTs, ↑NQO1 |
(36–38) |
| Cytoprotective | The antioxidative potential of sulforaphane enhanced the production and activity of cytoprotective proteins to help protect the cell lining ↑cellular defense mechanisms, ↑detoxification, ↑redox reactions, ↑Nrf2 |
(32, 33) |
| Immunostimulant | Immune booster, ↑NK cell activity | (22) |
| Antimicrobial | ↓growth of various gram-positive and gram-negative bacteria by preventing pyocyanin production, biofilm formation, and quorum sensing highly effective against Helicobacter pylori | (39–42) |
| Anti-carcinogenesis | Nrf2 and TrxRs have a dual role in cancer by protecting against oxidative stress. However, overactivation can promote tumor growth and may cause chemoresistance. Therefore, sulforaphane dosage must be selected carefully | (43–49) |
↑, increase; ↓, decrease; Nrf2, nuclear transcription factor; TRxRS, thioredoxin reductase; GSH, glutathione; GR, glutathione reductase; GSTs, glutathione-S transferase; NADPH, nicotinamide adenine dinucleotide phosphate; NQO1, NAD(P)H quinone oxidoreductase; NK cells, natural killer cells.