Clinical oral investigations · 2025
MALAT1/miR-181b axis mediates the anti-bacterial and anti-inflammatory effects of Galla chinensis in the progression of dental caries : Short title: mechanism of Galla chinensis in dental caries.
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Liu Yao, Min Qian, Lu Hongyan, Yi Feng, Li Ke
Аннотация
BACKGROUND: Dental caries is a common oral disease that seriously affects the oral health and quality of life of patients. The aim of this study is to investigate the anti-bacterial and anti-inflammatory effects of Galla chinensis (GC) in dental caries, and explore the underlying mechanisms based on non-coding RNAs.
METHODS: Mouse and cell models were established by bacterial infection method and LPS induction. The growth of Streptococcus mutans (S. mutans) was detected by growth curves and acid production experiments. ELISA was used to evaluated inflammatory responses, and the effect of GC on the viability of human dental pulp stem cells (HDPSCs) was analyzed by CCK-8 assay. The regulation of MALAT1 and miR-181b expression by GC was detected by qRT-PCR, and the role of the MALAT1/miR-181b axis in the function of GC was examined using rescue experiments by assessing cell and bacterial viability, inflammation and S. mutans infection.
RESULTS: GC significantly inhibited the growth and acid production of S. mutans, the levels of inflammatory factors and MALAT1 levels, and promoted miR-181b expression in both cell and animal models. Additionally, the proliferation of disease cell model was elevated by GC. miR-181b as a target of MALAT1, was inhibited by MALAT1 in cell model, and the MALAT1/miR-181b axis was found to mediate the regulatory effects of GC on S. mutans growth, infection-induced inflammatory, HDPSC viability and inflammation.
CONCLUSIONS: GC inhibits S. mutans growth and inflammatory responses in cells and animal models through the MALAT1/miR-181b axis. This study highlights the potential clinical value of targeting the MALAT1/miR-181b axis with GC, which may offer a novel therapeutic strategy for the prevention and treatment of dental caries in clinical practice.
METHODS: Mouse and cell models were established by bacterial infection method and LPS induction. The growth of Streptococcus mutans (S. mutans) was detected by growth curves and acid production experiments. ELISA was used to evaluated inflammatory responses, and the effect of GC on the viability of human dental pulp stem cells (HDPSCs) was analyzed by CCK-8 assay. The regulation of MALAT1 and miR-181b expression by GC was detected by qRT-PCR, and the role of the MALAT1/miR-181b axis in the function of GC was examined using rescue experiments by assessing cell and bacterial viability, inflammation and S. mutans infection.
RESULTS: GC significantly inhibited the growth and acid production of S. mutans, the levels of inflammatory factors and MALAT1 levels, and promoted miR-181b expression in both cell and animal models. Additionally, the proliferation of disease cell model was elevated by GC. miR-181b as a target of MALAT1, was inhibited by MALAT1 in cell model, and the MALAT1/miR-181b axis was found to mediate the regulatory effects of GC on S. mutans growth, infection-induced inflammatory, HDPSC viability and inflammation.
CONCLUSIONS: GC inhibits S. mutans growth and inflammatory responses in cells and animal models through the MALAT1/miR-181b axis. This study highlights the potential clinical value of targeting the MALAT1/miR-181b axis with GC, which may offer a novel therapeutic strategy for the prevention and treatment of dental caries in clinical practice.