Periodontitis is a series of inflammatory processes caused by bacterial infection. Parathyroid hormone (PTH) plays a critical role in bone remodeling. This study aimed to investigate the influences of PTH on human bone marrow mesenchymal stem cells (HBMSCs) pretreated with lipopolysaccharide (LPS). The proliferative ability was measured using cell counting kit-8 and flow cytometry. The optimal concentrations of PTH and LPS were determined using alkaline phosphatase (ALP) activity assay, ALP staining, and Alizarin red staining. Osteogenic differentiation was further assessed by quantitative reverse transcription-polymerase chain reaction, Western blot analysis, and immunofluorescence staining. PTH had no effects on the proliferation of HBMSCs. Also, 100 ng/mL LPS significantly inhibited HBMSC osteogenesis, while 10-9 mol/L PTH was considered as the optimal concentration to reverse the adverse effects. Mechanistically, c-Jun N-terminal kinase (JNK) phosphorylation was activated by PTH in LPS-induced HBMSCs. SP600125, a selective inhibitor targeting JNK mitogen-activated protein kinase (MAPK) signaling, weakened the effects of PTH. Taken together, the findings revealed the role and mechanism of PTH and JNK pathway in promoting the osteogenic differentiation of LPS-induced HBMSCs, which offered an alternative for treating periodontal diseases.

中文翻译：

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甲状旁腺激素通过 JNK MAPK 通路促进脂多糖诱导的人骨髓间充质干细胞的成骨。

牙周炎是由细菌感染引起的一系列炎症过程。甲状旁腺激素 (PTH) 在骨重塑中起关键作用。本研究旨在探讨 PTH 对经脂多糖 (LPS) 预处理的人骨髓间充质干细胞 (HBMSCs) 的影响。使用细胞计数试剂盒8和流式细胞术测量增殖能力。使用碱性磷酸酶 (ALP) 活性测定、ALP 染色和茜素红染色确定 PTH 和 LPS 的最佳浓度。通过定量逆转录聚合酶链反应、蛋白质印迹分析和免疫荧光染色进一步评估成骨分化。PTH对HBMSCs的增殖没有影响。此外，100 ng/mL LPS 显着抑制 HBMSC 成骨，而10-9 mol/L PTH被认为是逆转不良反应的最佳浓度。从机制上讲，LPS 诱导的 HBMSCs 中的 PTH 激活了 c-Jun N 末端激酶 (JNK) 磷酸化。SP600125 是一种靶向 JNK 丝裂原活化蛋白激酶 (MAPK) 信号传导的选择性抑制剂，可减弱 PTH 的作用。综上所述，该研究结果揭示了 PTH 和 JNK 通路在促进 LPS 诱导的 HBMSCs 成骨分化中的作用和机制，为治疗牙周病提供了另一种选择。