Spilanthol Inhibits COX-2 and ICAM-1 Expression via Suppression of NF-κB and MAPK Signaling in Interleukin-1β-Stimulated Human Lung Epithelial Cells.

Abstract

Spilanthol a phytochemical derived from the Spilanthes acmella plant has antimicrobial, antioxidant, and anti-inflammatory properties. This study evaluated its effects on the expression of intercellular adhesion molecule 1 (ICAM-1) and inflammation-related mediators in IL-1β-stimulated human lung epithelial A549 cells. Human lung epithelial A549 cells were pretreated with various concentrations of spilanthol (3-100 μM) followed by treatment with IL-1β to induce inflammation. The protein levels of pro-inflammatory cytokines, chemokines, and prostaglandin E2 (PGE2) were measured using ELISA. Cyclooxygenase-2 (COX-2), heme oxygenase (HO-1), nuclear transcription factor kappa-B (NF-κB), and mitogen-activated protein kinase (MAPK) were measured by immunoblotting. The mRNA expression levels of ICAM-1 and MUC5AC were determined by real-time polymerase chain reaction. Spilanthol decreased the expression of PGE2, COX-2, TNF-α, and MCP-1. It also decreased ICAM-1 expression and suppressed monocyte adhesion to IL-1β-stimulated A549 cells. Spilanthol also significantly inhibited the phosphorylation of MAPK and I-κB. These results suggest that spilanthol exerts anti-inflammatory effects by inhibiting the expression of the pro-inflammatory cytokines, COX-2, and ICAM-1 by inhibiting the NF-κB and MAPK signaling pathways. Graphical Abstract ᅟ.

• Authors: Wen-Chung Huang, Ling-Yu Wu, Sindy Hu, Shu-Ju Wu
• Journal: Inflammation (Inflammation) Vol. 41 Issue 5 Pg. 1934-1944 (Oct 2018) ISSN: 1573-2576 [Electronic] United States
• PMID: 29959625 (Publication Type: Journal Article)

Chemical References

• Anti-Inflammatory Agents
• Inflammation Mediators
• Interleukin-1beta
• N-isobutyl-2E-decenamide
• NF-kappa B
• Polyunsaturated Alkamides
• Intercellular Adhesion Molecule-1
• Cyclooxygenase 2
• Mitogen-Activated Protein Kinases

Topics

• A549 Cells
• Anti-Inflammatory Agents (pharmacology)
• Cyclooxygenase 2 (drug effects, metabolism)
• Epithelial Cells (metabolism)
• Humans
• Inflammation Mediators (metabolism)
• Intercellular Adhesion Molecule-1 (drug effects, metabolism)
• Interleukin-1beta (pharmacology)
• Mitogen-Activated Protein Kinases (antagonists & inhibitors)
• NF-kappa B (antagonists & inhibitors)
• Phosphorylation (drug effects)
• Polyunsaturated Alkamides (pharmacology)
• Signal Transduction (drug effects)