Kaempferol-3-o-β-d-glucuronate exhibit potential anti-inflammatory effect in LPS stimulated RAW 264.7 cells and mice model
Kaempferol-3-O-β-d-glucuronide (K3G) having various pharmacological effects was explored for its anti-inflammatory effect in LPS induced RAW 264.7 cells and mice model. K3G significantly inhibited various pro-inflammatory mediators like IL-1β, NO, PGE2, and LTB4. It upregulated the secretion of anti...
Gespeichert in:
Veröffentlicht in: | International immunopharmacology 2018-04, Vol.57, p.62-71 |
---|---|
Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Kaempferol-3-O-β-d-glucuronide (K3G) having various pharmacological effects was explored for its anti-inflammatory effect in LPS induced RAW 264.7 cells and mice model. K3G significantly inhibited various pro-inflammatory mediators like IL-1β, NO, PGE2, and LTB4. It upregulated the secretion of anti-inflammatory cytokine IL-10. K3G is found to reduce inflammation when studied for parameters like phagocytic index, carrageenan induced paw edema in mice and organ weight. It reduced inflammation in a dose dependent manner both in-vitro and in-vivo. Further molecular insights into the study reveal that K3G blocks the phosphorylation of NF-kB which is key regulator of inflammation, thereby exhibiting anti-inflammatory potential. Hence, this study permits further investigation to develop K3G as anti-inflammatory drug.
[Display omitted]
•K3G inhibited pro-inflammatory mediators IL-1β, NO, PGE2, LTB4 and upregulated anti-inflammatory cytokine IL-10.•K3G reduced inflammation when studied for parameters like phagocytic index and carrageenan induced paw edema in mice.•K3G exerts its effect by NF-kB suppression•Anti-inflammatory effect has been proved both in-vitro and in-vivo.•All this data permit K3G to be established as an anti-inflammatory drug. |
---|---|
ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2018.01.041 |