Hatakabb, a herbal extract, contains pyrogallol as the novel mediator inhibiting LPS-induced TNF-α production by NF-κB inactivation and HMOX-1 upregulation

Abstract

Hatakabb is a herbal extract traditionally consumed to ameliorate inflammation from pharynx infections. However, the anti-inflammatory function of Hatakabb was not investigated. This study demonstrated the anti-inflammatory potential, and underlying mechanism of Hatakabb, and its functional ingredient. In LPS-treated macrophages, Hatakabb treatment attenuated TNF-α production. A decrease in TNF-α, IL-6, and COX-2 expression was detected. In regulatory pathway analysis, Hatakabb suppressed IκB-α phosphorylation in accordance with a decrease in IκB-α degradation, and nucleus NF-κB translocation, while enhanced NF-κB phosphorylation. In addition, MAPK phosphorylation was enhanced in association with HMOX-1 upregulation. Our metabolomic analysis showed gallic acid, and pyrogallol contained in the anti-inflammatory subfraction. Compared to gallic acid, pyrogallol strongly diminished TNF-α production. Significant changes in inflammatory gene expression, and regulatory protein phosphorylation were responded to pyrogallol in similar to Hatakabb treatment. Our study, for the first time, reveals the anti-inflammatory effect, and mechanism of Hatakabb in which pyrogallol is the novel mediator inhibiting LPS-induced inflammation.