2. Academic Validation
  3. Baicalin attenuates LPS-induced periodontal inflammation response by inhibiting autophagy

Baicalin attenuates LPS-induced periodontal inflammation response by inhibiting autophagy

  • BMC Oral Health. 2025 Apr 10;25(1):513. doi: 10.1186/s12903-025-05913-7.
Yifan Cheng 1 2 3,  Ming Jiang 1 2 3,  Xu Qin 1 2 3,  Jing Mao 4 5 6,  Yan Liu 7,  Guangxun Zhu 8 9 10
Affiliations

Affiliations

  • 1 Department of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 2 School of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  • 3 Hubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration Wuhan, 430030, Hubei, China.
  • 4 Department of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. maojing@hust.edu.cn.
  • 5 School of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. maojing@hust.edu.cn.
  • 6 Hubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration Wuhan, 430030, Hubei, China. maojing@hust.edu.cn.
  • 7 Central Laboratory, Peking University School and Hospital for Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health & NMPA Key Laboratory for Dental Materials & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, 100081, China. orthoyan@bjmu.edu.cn.
  • 8 Department of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. zhuguangxun@163.com.
  • 9 School of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. zhuguangxun@163.com.
  • 10 Hubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration Wuhan, 430030, Hubei, China. zhuguangxun@163.com.
PMID: 40211339 DOI: 10.1186/s12903-025-05913-7
Abstract

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.

Keywords

Autophagy; Baicalin; Inflammation; Network Pharmacology; Periodontal disease; Transcriptomic sequencing analysis.

Figures
Products
Inhibitors & Agonists
Other Products