Xiang Yulan, Li Zelu, He Xin, Chu Xiaoyang, Gao Chunyan, Guo Jiahao, Luan Yingyi, Yang Kai, Zhang Dongliang
Department of Orthodontics, Beijing Stomatological Hospital, School of Stomatology, Capital Medical University, Capital Medical University, Beijing, China.
Department of Stomatology, Fifth Medical Center of Chinese PLA General Hospital, Beijing, China.
Stem Cell Res Ther. 2025 May 1;16(1):218. doi: 10.1186/s13287-025-04355-w.
Puerarin (Pue) has recently been reported to have therapeutic effects on periodontitis (PD). However, there is insufficient evidence, and the mechanism involved has not yet been revealed. This work delved to explore the exact therapeutic effects and molecular mechanism of Pue in treating PD.
PD mouse (C57BL/6 N mouse) model constructed by Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) induction was treated with Pue. Therapeutic efficacy of Pue for PD was examined by a series of experiments. PD cell model was induced by treating human periodontal ligament cells with Pg-LPS. Therapeutic effects of Pue on PD cell model, along with the potential molecular mechanism, were explored by logical experiments. Rescue experiments based on in vitro and in vivo studies were implemented to validate the molecular mechanism of Pue in treating PD.
In PD mice, Pue treatment relieved inflammation and bone destruction, facilitated osteogenic differentiation and autophagy in periapical tissues. In PD cell model, Pue treatment facilitated osteogenic differentiation and mitochondrial autophagy; suppressed inflammation and mitochondrial reactive oxygen species; maintained mitochondrial membrane potential and mitochondrial kinetic homeostasis; and activated mitochondrial Mitofusin 2 (Mfn2). However, these influences of Pue on PD cell model were eliminated by CsA (mitochondrial autophagy inhibitor). The enhanced mitochondrial autophagy induced by Pue was reversed by Mfn2 silencing. Through in vivo data, Mfn2 knockdown counteracted the therapeutic effects of Pue on PD mice.
Pue exerted therapeutic effects on PD, possibly by enhancing mitochondrial autophagy via activating mitochondrial Mfn2. This might be a cure for PD.
近期有报道称葛根素（Pue）对牙周炎（PD）具有治疗作用。然而，证据尚不充分，其相关机制也尚未明确。本研究旨在探究葛根素治疗牙周炎的确切治疗效果及分子机制。
用牙龈卟啉单胞菌脂多糖（Pg-LPS）诱导构建的PD小鼠（C57BL/6 N小鼠）模型接受葛根素治疗。通过一系列实验检测葛根素对PD的治疗效果。用Pg-LPS处理人牙周膜细胞诱导建立PD细胞模型。通过逻辑实验探究葛根素对PD细胞模型的治疗效果及其潜在分子机制。基于体外和体内研究进行挽救实验，以验证葛根素治疗PD的分子机制。
在PD小鼠中，葛根素治疗可减轻炎症和骨破坏，促进根尖周组织的成骨分化和自噬。在PD细胞模型中，葛根素治疗可促进成骨分化和线粒体自噬；抑制炎症和线粒体活性氧；维持线粒体膜电位和线粒体动力学稳态；并激活线粒体融合蛋白2（Mfn2）。然而，CsA（线粒体自噬抑制剂）消除了葛根素对PD细胞模型的这些影响。Mfn2沉默逆转了葛根素诱导的增强的线粒体自噬。通过体内数据，Mfn2基因敲低抵消了葛根素对PD小鼠的治疗效果。
葛根素对PD具有治疗作用，可能是通过激活线粒体Mfn2增强线粒体自噬来实现的。这可能是一种治疗PD的方法。
