BMC oral health · 2025
Baicalin attenuates LPS-induced periodontal inflammation response by inhibiting autophagy.
СтатьяНазвание и аннотация: Перевод в очереди
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Cheng Yifan, Jiang Ming, Qin Xu, Mao Jing, Liu Yan, Zhu Guangxun
Аннотация
BACKGROUND: Periodontal disease causes gradual damage to the periodontal ligament and alveolar bone, ultimately resulting in tooth loss. This condition This condition results from the intricate interaction between bacterial infections and the host's inflammatory responses, driving disease progression. Autophagy, an essential process for cellular balance under stress, plays a vital role in the response to periodontal pathogens. Baicalin (BA), a flavonoid extracted from Scutellaria baicalensis, is recognized for its potent anti-inflammatory effects. However, its influence on autophagy in periodontal health is not fully characterized, representing a vital gap in therapeutic understanding.
PURPOSE: This study investigates the therapeutic potential of BA in periodontal disease by examining its regulatory effects on autophagy and inflammation in PDLCs.
METHODS: Periodontal ligament cells (PDLCs) were exposed to various concentrations of BA, and cell proliferation was measured using the CCK-8 assay. Anti-inflammatory responses were analyzed by quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Autophagy levels were quantified using immunofluorescence, transmission electron microscopy (TEM), and Western blotting. To identify potential targets of BA, an integrated approach combining network pharmacology and RNA sequencing (RNA-Seq) was employed. These analyses were subsequently validated using qRT-PCR, molecular docking and dynamics simulations.
RESULTS: BA significantly reduced lipopolysaccharide (LPS)-induced inflammatory responses in PDLCs, as evidenced by a decrease in the levels of interleukin (IL)-1β and IL-6. RNA-Seq analysis indicated that these effects were associated with autophagy-related processes. Notably, BA decreased Beclin-1 levels, reduced the LC3BII/I ratio, diminished LC3B protein staining, and decreased the number of autophagosomes. Furthermore, BA triggered the activation of the PI3K/AKT/mTOR pathway, demonstrated by the increased phosphorylation of these proteins.
CONCLUSION: BA acts as a protective agent against LPS-induced periodontal inflammation by modulating autophagy, positioning it as a promising candidate for future periodontal therapies.
PURPOSE: This study investigates the therapeutic potential of BA in periodontal disease by examining its regulatory effects on autophagy and inflammation in PDLCs.
METHODS: Periodontal ligament cells (PDLCs) were exposed to various concentrations of BA, and cell proliferation was measured using the CCK-8 assay. Anti-inflammatory responses were analyzed by quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Autophagy levels were quantified using immunofluorescence, transmission electron microscopy (TEM), and Western blotting. To identify potential targets of BA, an integrated approach combining network pharmacology and RNA sequencing (RNA-Seq) was employed. These analyses were subsequently validated using qRT-PCR, molecular docking and dynamics simulations.
RESULTS: BA significantly reduced lipopolysaccharide (LPS)-induced inflammatory responses in PDLCs, as evidenced by a decrease in the levels of interleukin (IL)-1β and IL-6. RNA-Seq analysis indicated that these effects were associated with autophagy-related processes. Notably, BA decreased Beclin-1 levels, reduced the LC3BII/I ratio, diminished LC3B protein staining, and decreased the number of autophagosomes. Furthermore, BA triggered the activation of the PI3K/AKT/mTOR pathway, demonstrated by the increased phosphorylation of these proteins.
CONCLUSION: BA acts as a protective agent against LPS-induced periodontal inflammation by modulating autophagy, positioning it as a promising candidate for future periodontal therapies.