Diabetes mellitus (DM)‐induced glucolipotoxicity is a factor strongly contributing to alveolar bone deficiency. Parathyroid hormone (PTH) has been identified as a main systemic mediator to balance physiological calcium in bone. This study aimed to uncover PTH's potential role in ameliorating the osteogenic capacity of human bone marrow mesenchymal stem cells (HBMSCs) against glucolipotoxicity. Optimal PTH concentrations and high glucose and palmitic acid (GP) were administered to cells, followed by alkaline phosphatase (ALP) staining and ALP activity assay. Quantitative real‐time reverse transcription‐polymerase chain reaction (qRT‐PCR) and Immunoblot were carried out for assessing mRNA and protein amounts, respectively. Cell counting kit‐8 (CCK‐8) and flow cytometry were performed for quantitating cell proliferation. Osteogenesis and oxidative stress were determined, and the involvement of mitogen‐activated protein kinase (MAPK) signaling was further verified. About 1–50 mmol/ml GP significantly inhibited the osteogenic differentiation of HBMSCs. 10−9 mol/L PTH was found to be the optimal concentration for HBMSC induction. PTH had no effects on HBMSC proliferation, with or without GP treatment. PTH reversed inadequate osteogenesis and excessive oxidative stress in GP‐treated HBMSCs. Mechanistically, PTH activated p38 MAPK signaling, while inhibiting p38 MAPK‐suppressed PTH's beneficial impacts on HBMSCs. Collectively, PTH promotes osteogenic differentiation in HBMSCs against glucolipotoxicity via p38 MAPK signaling.

中文翻译：

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甲状旁腺激素通过 p38 MAPK 信号通路改善人骨髓间充质干细胞的成骨抗糖脂毒性

糖尿病（DM）诱导的糖脂毒性是导致牙槽骨缺乏的一个重要因素。甲状旁腺激素 (PTH) 已被确定为平衡骨中生理钙的主要全身介质。本研究旨在揭示 PTH 在改善人骨髓间充质干细胞 (HBMSCs) 抗糖脂毒性的成骨能力中的潜在作用。向细胞施用最佳 PTH 浓度和高葡萄糖和棕榈酸 (GP)，然后进行碱性磷酸酶 (ALP) 染色和 ALP 活性测定。定量实时逆转录聚合酶链反应 (qRT-PCR) 和免疫印迹分别用于评估 mRNA 和蛋白质的量。细胞计数试剂盒-8 (CCK-8) 和流式细胞仪用于定量细胞增殖。确定了成骨和氧化应激，并进一步验证了丝裂原活化蛋白激酶 (MAPK) 信号传导的参与。约 1-50 mmol/ml GP 显着抑制 HBMSCs 的成骨分化。发现 10-9 mol/L PTH 是 HBMSC 诱导的最佳浓度。PTH 对 HBMSC 增殖没有影响，无论有没有 GP 治疗。PTH 逆转了 GP 治疗的 HBMSCs 的成骨不足和过度氧化应激。从机制上讲，PTH 激活 p38 MAPK 信号，同时抑制 p38 MAPK 抑制 PTH 对 HBMSCs 的有益影响。总的来说，PTH 通过 p38 MAPK 信号传导促进 HBMSCs 中的成骨分化对抗糖脂毒性。约 1-50 mmol/ml GP 显着抑制 HBMSCs 的成骨分化。发现 10-9 mol/L PTH 是 HBMSC 诱导的最佳浓度。PTH 对 HBMSC 增殖没有影响，无论有没有 GP 治疗。PTH 逆转了 GP 治疗的 HBMSCs 的成骨不足和过度氧化应激。从机制上讲，PTH 激活 p38 MAPK 信号，同时抑制 p38 MAPK 抑制 PTH 对 HBMSCs 的有益影响。总的来说，PTH 通过 p38 MAPK 信号传导促进 HBMSCs 中的成骨分化对抗糖脂毒性。约 1-50 mmol/ml GP 显着抑制 HBMSCs 的成骨分化。发现 10-9 mol/L PTH 是 HBMSC 诱导的最佳浓度。PTH 对 HBMSC 增殖没有影响，无论有没有 GP 治疗。PTH 逆转了 GP 治疗的 HBMSCs 的成骨不足和过度氧化应激。从机制上讲，PTH 激活 p38 MAPK 信号，同时抑制 p38 MAPK 抑制 PTH 对 HBMSCs 的有益影响。总的来说，PTH 通过 p38 MAPK 信号传导促进 HBMSCs 中的成骨分化对抗糖脂毒性。PTH 逆转了 GP 治疗的 HBMSCs 的成骨不足和过度氧化应激。从机制上讲，PTH 激活 p38 MAPK 信号，同时抑制 p38 MAPK 抑制 PTH 对 HBMSCs 的有益影响。总的来说，PTH 通过 p38 MAPK 信号传导促进 HBMSCs 中的成骨分化对抗糖脂毒性。PTH 逆转了 GP 治疗的 HBMSCs 的成骨不足和过度氧化应激。从机制上讲，PTH 激活 p38 MAPK 信号，同时抑制 p38 MAPK 抑制 PTH 对 HBMSCs 的有益影响。总的来说，PTH 通过 p38 MAPK 信号传导促进 HBMSCs 中的成骨分化对抗糖脂毒性。