Archives of oral biology · 2026
Investigating the mechanism of berberine in inhibiting periodontitis progression using machine learning, molecular docking, and experimental validation.
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Wang Zhonghua, Liu Zhenli, Ma Sai, Jia Xiaohui, Zhang Xu, Zhang Zhiyi, Li Chao, Xiao Jinping, Si Yan
Аннотация
BACKGROUND: Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissues. Berberine (BBR), a natural alkaloid with anti-inflammatory and antioxidant properties, has shown potential in treating inflammatory diseases.
METHODS: Differentially expressed genes (DEGs) between periodontitis and healthy gingival tissues were identified using the GSE23586 and GSE173078 datasets, while chronic periodontitis-related genes were retrieved from the GeneCards database. Key genes were screened through support vector machine (SVM) and random forest (RF) algorithms, molecular docking, and normal mode analysis. In vitro, human gingival fibroblast-1 (HGF-1) cells were treated with lipopolysaccharide (LPS) to simulate periodontitis.
RESULTS: Six key genes (KRT14, IGFBP6, LRG1, MZB1, DEFB103A, and CD79A) were identified by both SVM and RF algorithms. LRG1 was selected for further study due to its significant downregulation after BBR treatment in LPS-treated HGF-1 cells. LPS treatment increased LRG1 expression and the p-p38/p38 ratio, whereas these effects reversed by BBR treatment. Overexpression of LRG1 diminished BBR's inhibitory effect on p-p38/p38, while the p38 MAPK pathway inhibitor restored BBR's efficacy. BBR treatment suppressed LPS-induced inflammatory response, oxidative stress, and ECM degradation, but these effects were relieved by ectopic LRG1 expression.
CONCLUSION: BBR alleviated LPS-induced periodontitis by inhibiting inflammation, oxidative stress, and ECM degradation through inactivation of the LRG1/p38 MAPK signaling pathway. These findings highlight BBR's potential as a therapeutic agent for periodontitis, offering a novel molecular target for clinical intervention. Further in vivo studies are warranted to validate its clinical application.
METHODS: Differentially expressed genes (DEGs) between periodontitis and healthy gingival tissues were identified using the GSE23586 and GSE173078 datasets, while chronic periodontitis-related genes were retrieved from the GeneCards database. Key genes were screened through support vector machine (SVM) and random forest (RF) algorithms, molecular docking, and normal mode analysis. In vitro, human gingival fibroblast-1 (HGF-1) cells were treated with lipopolysaccharide (LPS) to simulate periodontitis.
RESULTS: Six key genes (KRT14, IGFBP6, LRG1, MZB1, DEFB103A, and CD79A) were identified by both SVM and RF algorithms. LRG1 was selected for further study due to its significant downregulation after BBR treatment in LPS-treated HGF-1 cells. LPS treatment increased LRG1 expression and the p-p38/p38 ratio, whereas these effects reversed by BBR treatment. Overexpression of LRG1 diminished BBR's inhibitory effect on p-p38/p38, while the p38 MAPK pathway inhibitor restored BBR's efficacy. BBR treatment suppressed LPS-induced inflammatory response, oxidative stress, and ECM degradation, but these effects were relieved by ectopic LRG1 expression.
CONCLUSION: BBR alleviated LPS-induced periodontitis by inhibiting inflammation, oxidative stress, and ECM degradation through inactivation of the LRG1/p38 MAPK signaling pathway. These findings highlight BBR's potential as a therapeutic agent for periodontitis, offering a novel molecular target for clinical intervention. Further in vivo studies are warranted to validate its clinical application.