Dataset Information

Proteomic analysis of periodontal tissue reveals β-guanidinopropionic acid (β-GPA) mediated inhibition of the TLR4 pathway in a mouse model of hyperlipidemic periodontitis.

ABSTRACT: This project aims to elucidate the molecular mechanisms by which the gut microbial metabolite β-guanidinopropionic acid (β-GPA) alleviates hyperlipidemic periodontitis (HPD). We performed Tandem Mass Tag (TMT) based quantitative proteomic analysis on periodontal tissues from HPD model mice versus those treated with β-GPA. The goal was to identify key differentially expressed proteins and uncover the protective signaling pathways modulated by β-GPA, ultimately identifying the TLR4-MyD88 axis as a primary therapeutic target.

ORGANISM(S): Mus Musculus

SUBMITTER: Min Hu

PROVIDER: PXD069376 | iProX | Mon Oct 13 00:00:00 GMT+01:00 2025

REPOSITORIES: iProX

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Publications

Gut commensal Odoribacter splanchnicus attenuates hyperlipidemic periodontitis via gut-oral metabolic transmission of β-GPA.

Xu Jing J Han Ziyi Z Xue Qing Q Wang Haoran H Li Yutong Y Song Jiyu J Li Lanzhou L Hu Min M Wang Di D

NPJ biofilms and microbiomes 20260611

Hyperlipidemic periodontitis (HPD) represents a prevalent comorbidity linking systemic metabolic dysregulation with local inflammation, yet the microbial mechanisms driving this gut-oral crosstalk remain elusive. Here, the comorbid state of HPD is linked to hyperlipidemia-associated gut microbiota changes, which are prominently accompanied by the depletion of Odoribacter splanchnicus in both patients and mice. Fecal microbiota transplantation demonstrates that this gut dysbiosis exacerbates peri ...[more]

PMID: 42277050

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Project description:Periodontitis (PD) as a chronic inflammatory disease instigated by periodontal pathogenic bacteria and mediated by the host immune response, resulting in the destruction of supporting periodontal tissue and tooth loss in adults. Constructing an injectable delivery system that allows for sustained drug release within periodontal pockets to continuously eliminate pathogenic bacteria, reduce periodontal inflammation, and promote periodontal tissue regeneration is an effective strategy for periodontitis treatment. Here, we explore the therapeutic potential and underlying mechanisms of curcumin-loaded Pickering emulsion (PE-CUR) in periodontitis treatment. The Pickering emulsion formulation offers an effective delivery system, enhancing curcumin's bioavailability and therapeutic efficacy. In vitro studies, we demonstrate that the PE-CUR exhibit excellent biocompatibility and anti-inflammatory property by elimination of reactive oxygen species (ROS). In addition, PE-CUR significantly eliminate key periodontal pathogens, including Porphyromonas gingivalis (P. gingivalis) and Staphylococcus aureus (S. aureus). In a rat model of periodontitis, PE-CUR significantly attenuates periodontal tissue inflammation and alveolar bone loss, indicating a protective effect against periodontal tissue destruction. Mechanistically, PE-CUR promotes the expression of anti-inflammatory factors and inhibits the release of pro-inflammatory factors by regulating macrophage polarization from M1 to M2 and modulating the MAPK and PI3K-AKT signaling pathway. Furthermore, PE-CUR decreases the formation of osteoclasts as well as stimulates the activation and differentiation of osteoblasts successively, thereby ameliorating the periodontal inflammation and promoting the alveolar bone regeneration. Overall, our findings elucidate the therapeutic mechanisms of PE-CUR in periodontitis, suggesting its potential as a promising treatment strategy warranting further clinical investigation.

Dataset Information

Proteomic analysis of periodontal tissue reveals β-guanidinopropionic acid (β-GPA) mediated inhibition of the TLR4 pathway in a mouse model of hyperlipidemic periodontitis.

Publications

Gut commensal Odoribacter splanchnicus attenuates hyperlipidemic periodontitis via gut-oral metabolic transmission of β-GPA.

Similar Datasets

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