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.
Highlights
Oncostatin M (OSM) is known as a tumor-related cytokine that exhibits high expression levels in cancer patients [1,2]
It has been known that high expression of OSM was exhibited in a wide r inflammatory diseases, inclusive of asthma and chronic rhinosinusitis [1 Upregulated mRNA expression of OSM resulted from stimulation with granulocyte-macrophage colony-stimulating factor (GM-CSF)
Our results showed that stimulation with recombinant human GM-CSF increases the production and mRNA expression of OSM (Figures 2a and 3) in ways consistent with a previous report [13]
Summary
Oncostatin M (OSM) is known as a tumor-related cytokine that exhibits high expression levels in cancer patients [1,2]. OSM is known as an inflammatory cytokine and is secreted from diverse cells, inclusive of T cells, monocytes, dendritic cells, macrophages, and neutrophils [3,4,5,6,7]. Cytokine OSM is regarded as an important factor in a variety of inflammatory reactions [2]. Stimulation with recombinant human OSM resulted in elevated expressions of inflammatory cytokine and chemokine in normal human colonic stromal cells [3]. Liu and colleagues adduced that recombinant human OSM treatment increases inflammatory cytokine interleukin (IL)-1β release from HaCaT cells [7]. Akt plays an ess inflammatory reactions as a downstream molecule of PI3K [15]. SCMhanigsanpdrocodllueacgeudesbsuyg-the PI3 gpeasttehdwthaayt th[1e5P,I23K1–/A23kt].siWgnaul peatthawl.a[y2i1s ]pirveoptaol rintethde tchytaotkiOneSsMignpalrinogdnuetcwtioorkn[1is6].mediat
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