Table 6.
The anti-inflammatory mechanism of silybin in other diseases.
| Diseases | Key associated effect | Regulated factors | Reference |
|---|---|---|---|
| TPA-induced skin inflammation | ↓ PI3K/Akt signaling pathway; ↓ NF-κB activation | ↓ PI3K/Akt signaling pathway, ↓ NF-κB activation, ↓ IL-1β, ↓ IL-6, ↓ TNF-α, ↓ COX-2, ↓ IKK | (81) |
| Psoriasis | ↓ PI3K/Akt/mTOR signaling pathway; ↓ activation of NF-κB | ↓ PI3K/Akt/mTOR signaling pathway,↓ KEAP 1, ↑ NRF 2, ↓ NF-κB signaling pathway,↓ IL-23, ↓ IL-17 A | (82) |
| HD-induced skin injury | ↓ AP-1/NF-κB dual signaling pathways; ↓ multiple pro-inflammatory mediators | ↓ COX-2, ↓ iNOS, ↓ MMP-9 | (83) |
| LPS-induced inflammation in human dermal fibroblasts | ↓ NF-κB DNA-binding activity | ↓ IL-6,↓ IL-8, | (84) |
| ↑ IL-8 mRNA; ↑ AP-1 signaling pathway | ↑ AP-1 signaling pathway | ||
| UVB-induced skin photodamage | ↓ NF-κB p50 pathway; ↑ DNA repair | p53, ↓ COX-2, ↓ iNOS, ↓ TNF-α, ↓ IL-6 | (85) |
| Photoaging | ↑ Phosphorylation of p-Smad2/3; ↑ collagen, and elastin deposition | ↓ CYP26B1, ↑ ECM | (86) |
| Glaucoma | Regulate the expression profiles of coding genes and non-coding RNAs, construct a ceRNA network, ↓ and extracellular matrix deposition, ↓ and fibrosis | ↓ TGF-β, ↓ PI3K-Akt signaling pathway, ↑ NF-κB signaling pathway | (87) |
| AMD | ↓ PI3K/Akt/mTOR/p70S6K signaling pathway; ↓ HIF-1α; ↓ VEGF | ↓ PI3K/Akt/mTOR/p70S6K signaling pathway, ↓ HIF-1α, ↓ VEGF | (88) |
| ↑ PHD2; ↓ interaction between HIF-1α and VHL; ↑ degradation of HIF-1α | ↑ PHD2 | (88, 89) | |
| Periodontitis | ↓ NF-κB/NLRP3 inflammasome signaling axis, ↓ pro-inflammatory cytokines; ↑ Nrf2 antioxidant pathway; ↓ oxidative stress; vicious cycle between inflammation and oxidative damage | ↓ NF-κB/NLRP3 inflammasome signaling axis,↓ TNF-α, ↓ IL-1β, ↓ IL-6, ↑ Nrf2 antioxidant pathway, | (92) |
“↑” represents silybin’s promoting effect. “↓” represents silybin’s inhibiting effect.