Ursolic Acid Suppresses Oncostatin M Expression through Blockade of PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells

Abstract

Cytokine oncostatin M (OSM) plays an important role in a variety of inflammatory reactions and is mainly produced in neutrophils in inflammatory diseases. While natural pentacyclic triterpenoid ursolic acid (UA) possesses a wide range of beneficial effects, such as anti-oxidant, anti-tumor, and anti-inflammatory, the regulatory processes of OSM suppression by UA in neutrophils are still poorly understood. This study was aimed at examining how UA regulates OSM expression in neutrophil-like differentiated (d)HL-60 cells. Enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, and immunoblotting were employed to analyze the effects of UA. Whereas stimulation with granulocyte-macrophage colony-stimulating factor (GM-CSF) led to elevations of OSM production and mRNA expression, these elevations were lowered by treatment with UA in neutrophil-like dHL-60 cells. When the cells were exposed to GM-CSF, phosphorylated levels of phosphatidylinositol 3-kinase, Akt, and nuclear factor-kB were upregulated. However, the upregulations were diminished by treatment with UA in neutrophil-like dHL-60 cells. The results of this study proposed that UA might relieve inflammatory diseases via inhibition of OSM.