Catalpol reduces the production of inflammatory mediators via PPAR-γ activation in human intestinal Caco-2 cells.

Catalpol, a major iridoid glycoside present in Rehmannia glutinosa, has been reported to show a variety of pharmacological properties. However, the molecular mechanism underlying the anti-inflammatory effect of catalpol in intestinal cells remains poorly understood. The present study was aimed at investigating the effects of catalpol on the production of inflammatory mediators and its underlying signaling pathways in human intestinal Caco-2 cells. Catalpol significantly inhibited IL-1β-induced mRNA synthesis and protein production of pro-inflammatory cytokines, including IL-6, IL-8, and MCP-1. Further investigation of the molecular mechanism revealed that the anti-inflammatory effect of catalpol in Caco-2 cells is similar to that of troglitazone-a synthetic peroxisome proliferator-activated receptor (PPAR)-γ agonist-on intestinal inflammation mediated by PPAR-γ activation. These findings suggest that the clinical application of medicinal plants that contain catalpol may lead to a partial prevention of intestinal inflammation.