# Protaetia brevitarsis seulensis Larvae Extract Attenuates Inflammatory Osteoclast Differentiation and Bone Loss

## TL;DR

This study shows that an extract from Protaetia brevitarsis seulensis larvae can reduce inflammation-related bone loss by inhibiting osteoclast formation.

## Contribution

The study identifies a novel food-derived extract with potential to manage inflammation-associated bone loss.

## Key findings

- PBE inhibited IL-1-induced osteoclast differentiation and reduced RANKL and PGE2 production.
- PBE suppressed osteoclastogenesis in precursors exposed to RANKL or TNF-α.
- In vivo, PBE reduced LPS-induced bone loss and associated RANKL and PGE2 increases.

## Abstract

Background/Objectives: The larvae of Protaetia brevitarsis seulensis (PB), an edible insect, exhibit diverse bioactivities, but their effects on inflammatory bone loss remain unclear. We investigated whether a 70% ethanol extract of PB larvae (PBE) suppresses osteoclast differentiation and bone loss under inflammatory conditions. Methods: Osteoclast differentiation was assessed in co-cultures of mouse bone marrow cells and osteocytic cells stimulated with interleukin-1 (IL-1). Direct effects on osteoclast precursors were tested in bone marrow–derived macrophages exposed to receptor activator of nuclear factor-κB ligand (RANKL) or tumor necrosis factor-α (TNF-α). Skeletal effects were evaluated in a mouse model of lipopolysaccharide (LPS)-induced bone loss. Results: PBE inhibited IL-1–induced osteoclast differentiation in co-culture, reduced osteocytic RANKL expression and prostaglandin E2 (PGE2) production, and dampened early IL-1 signaling. In osteoclast precursors, PBE directly suppressed osteoclastogenesis driven by RANKL or TNF-α. In vivo, PBE attenuated LPS-induced bone loss and blunted the associated increases in bone RANKL and PGE2. Conclusions: PBE limits inflammatory osteoclastogenesis by downregulating PGE2 and RANKL production in osteoclast-supporting cells and directly inhibiting osteoclast precursor differentiation, thereby attenuating LPS-induced bone loss. These findings identify PBE as a food-derived candidate for managing inflammation-associated bone loss and support further preclinical and nutritional intervention studies.