White-spotted flower chafer (Protaetia brevitarsis) ameliorates inflammatory responses in LPS-stimulated RAW 264.7 macrophages

White-spotted flower chafer (Protaetia brevitarsis) is an edible insect and P. brevitarsis larvae are used in traditional Oriental medicine. However, the molecular mechanisms behind the anti-inflammatory action of P. brevitarsis larvae are unknown. We investigated the effects of P. brevitarsis larvae ethanol extract (PBLE) on the inflammatory response as well as the molecular mechanisms underpinning this effect in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. PBLE effectively inhibited the synthesis of nitric oxide (NO) through inducible NO synthase (iNOS) and cyclooxygenase 2 protein expression and 20 mu M PBLE suppressed the expression of pro-inflammatory cytokines, including interleukin (IL)-6 and IL-8, at a dose of. Further investigation of the mechanisms revealed that PBLE attenuated phosphorylation of nuclear factor kappa B (NF-kappa B) inhibitor alpha (I kappa B-alpha) and NF-kappa B p65 and interfered selectively with extracellular signal-regulated kinase (ERK)1/2 and p38 phosphorylation. These findings provide the first molecular basis that PBLE could be a potential candidate for attenuating proinflammatory NO induction via selective inhibition of the NF-kappa B, ERK, and p38 mitogen-activated protein kinase signalling pathways. It is necessary to verify the anti-inflammatory action of PBLE and to ascertain the related mechanisms, both in in vivo models and in clinical studies, to enable the application of PBLE as a potential therapeutic agent for inflammatory diseases.

Automated summary

White-spotted flower chafer (Protaetia brevitarsis) is an edible insect used in traditional Oriental medicine. The study investigated the anti-inflammatory effects of P. brevitarsis larvae ethanol extract (PBLE) on lipopolysaccharide-stimulated macrophages and identified its molecular mechanisms. PBLE effectively inhibited the synthesis of nitric oxide and pro-inflammatory cytokines, potentially through selective inhibition of NF-kappa B, ERK, and p38 MAPK signaling pathways. Further research is needed to confirm and understand the anti-inflammatory actions of PBLE for potential therapeutic applications.