ArticleProbiotics and antimicrobial proteins2026
Lacticaseibacillus rhamnosus LGG Suppresses Osteoclastogenesis via TLR6/NF-κB Modulation and Attenuates Ovariectomy-Induced Bone Loss in Mice.
Article in Probiotics and antimicrobial proteins, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeting the gut-bone axis in osteoporosis: probiotic interventions and other microbiota-based therapeutic strategies.Gut microbes · 2026Review
- Anti-Cancer Outcome of Glucocorticoid Receptor Transrepression by Synephrine Derivatives in Hematological Malignancies.International journal of molecular sciences · 2025Article
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10 authors.
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Abstract
Osteoporosis is characterized by decreased bone mass and disrupted microarchitecture. Gut microbiota-derived factors may regulate bone homeostasis. This study investigated the effects and mechanisms of Lacticaseibacillus rhamnosus LGG, conditioned medium (LCM) on osteoclastogenesis and bone loss. RANKL-induced osteoclast differentiation in bone marrow-derived macrophages (BMMs) was assessed by TRAP staining, F-actin ring imaging, resorption pit assay, qRT-PCR, and Western blotting. Ovariectomized (OVX) mice received oral LCM for 8 weeks. Bone architecture was analyzed by micro-CT and histology (H&E, TRAP, immunohistochemistry). Serum bone turnover markers and toxicity indicators were measured by ELISA. Transcriptome sequencing was performed on LCM-treated BMMs, followed by differential expression and KEGG enrichment analyses. Pathway involvement was validated via pharmacological inhibition. LCM demonstrated favorable biocompatibility while significantly reducing TRAP-positive cell number, F-actin ring formation, and bone resorption area in RANKL-treated BMMs. The expression of osteoclastogenic markers was markedly downregulated. In OVX mice, LCM treatment preserved the trabecular microarchitecture of lumbar vertebrae and femur, increased BV/TV, Tb.Th, and Tb.N, and reduced osteoclast number. Serum bone resorption marker (β-CTx) decreased, while bone formation markers (BALP and P1NP) showed no significant change. No adverse effects were observed in body weight or liver and kidney function indices. Transcriptome analysis revealed NF-κB pathway suppression. Western blotting confirmed that LCM reduced phosphorylation of IKKα, IκBα, and p65. Regulation of TLR6 can restore NF-κB activation and osteoclast function. LCM alleviates bone loss by inhibiting osteoclastogenesis mediated via the TLR6/NF-κB signaling pathway. LGG shows promise as a potential therapeutic agent, warranting further clinical investigation.
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