Abstract
Inflammation is important and has been found to be an underlying cause in many acute and chronic human diseases. Nuciferine, a natural alkaloid containing an aromatic ring, is found in the nelumbo nucifera leaves. It has been shown to have potential anti-inflammatory activities, but the molecular mechanism has remained unclear. In this study, we found that nuciferine (10 μM) significantly inhibited the lipopolysaccharide (LPS)-induced inflammatory cytokine IL-6 and TNF-α production in RAW 264.7 cells. In addition, the luciferase reporter assay results of different subtypes of the peroxisome proliferator-activated receptor (PPAR) showed that nuciferine dose-dependently activated all the PPAR activities. Specific inhibitors of PPARα and PPARγ significantly abolished the production of inflammatory cytokines as well as IκBα degradation. However, PPARδ inhibitor did not show this effect. Our results suggested a potential molecular mechanism of the anti-inflammatory effects of nuciferine in LPS-induced inflammation, at least in part, by activating PPARα and PPARγ in RAW 264.7 cells.
Highlights
Inflammatory responses are widely implicated in vast kinds of acute and chronic human diseases, including cancer, atherosclerosis, and diabetes [1]
peroxisome proliferator-activated receptor (PPAR) and the differences of the distinct tissue-specific expression, physiology, and ligand specificity of investigate the effect of nuciferine on inflammation in lipopolysaccharide (LPS)-induced RAW264.7 the PPARα, PPARβ/δ, and the PPARγ, the aim of this study was to investigate the effect of nuciferine cells and to observe if this effect is mediated by the three PPAR subtypes
The results suggested that nuciferine dramatically inhibited the LPS-induced nuclear factor-κB (NF-κB) activation and its effect was PPARs-dependent
Summary
Inflammatory responses are widely implicated in vast kinds of acute and chronic human diseases, including cancer, atherosclerosis, and diabetes [1]. Macrophages play a critical role and are involved in the self-regulating cycle of inflammation, as macrophages produce multiple pro-inflammatory cytokines and mediators that are involved in inflammation, such as the TNFα and the IL-6 [2]. Regulation of the inflammatory response depends on a variety of potential mechanisms, including peroxisome proliferator-activated receptors (PPARs) actions [3]. PPARs are activated by their synthetic or natural ligands/modulators, which lead to the PPARs to bind to their specific DNA response elements, as heterodimers, with the retinoid X receptor (RXR) [4]. PPARs have been found to have three subtypes, which are named PPARα, PPARβ/δ, and PPAR. They play crucial roles in the regulation of lipid and glucose metabolism. Accumulating evidence reveals that activation of the PPARs
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