反应性氧物种 (ROS) 驱动糖尿病骨质疏松症中骨细胞功能障碍,通过损害自和触发亡
Mengqi Han1,2, Minyue Zhao1,2, Furong Bai1,2
1Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an 710004, China.
Antioxidants (Basel, Switzerland)
|November 27, 2025
概括
高葡萄糖通过增加氧化应激和抑制自而损害骨细胞,导致亡. 针对反应性氧物种和自途径的疗法可以治疗糖尿病骨质疏松症.
科学领域:
- 生物医学科学 生物医学科学
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 糖尿病骨质疏松症是2型糖尿病 (T2DM) 的常见并发症.
- 在T2DM中高血糖会通过反应性氧物种 (ROS) 生产诱导氧化应激,损害骨细胞并加速骨质流失.
研究的目的:
- 在高葡萄糖 (HG) 环境中研究骨细胞损伤的机制.
- 探索糖尿病骨质疏松症的治疗目标和诊断标记.
主要方法:
- 在正常和HG条件下培养的MLO-Y4细胞和初级小鼠骨细胞.
- 用N-乙半氨酸 (NAC) 和拉帕米辛治疗的细胞.
- 通过各种测试 (CCK8,流细胞计,西斑,qRT-PCR,免疫光,TUNEL染色) 来评估细胞活力,ROS,自和亡标记.
主要成果:
- HG抑制了细胞增殖,诱导了胰岛素抵抗,增加了ROS,并促进了氧化应激.
- HG导致了mTOR激活,自抑制和骨细胞亡.
- 纳克减轻了HG诱导的损伤;拉巴素通过促进自和抑制mTOR来预防亡.
结论:
- 由ROS诱导的mTOR激活会损害自,阻碍损坏的骨细胞清除并触发亡.
- 这些发现提供了糖尿病骨质疏松病变的证据,并建议针对ROS和自的潜在治疗策略.
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