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阿斯素通过激活Nrf2/ARE通路来逆转人类牙周结节干细胞中氧化压力诱导的功能障碍
Jingwen Chi1,2, Xiaofei Yu1,2,3, Hui Zhang1,2,3
1Department of Stomatology, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China, qdu.edu.cn.
Stem cells international
|January 26, 2026
概括
阿斯坦丁 (ASX) 通过减少活性氧物种 (ROS) 和炎症来保护人类牙周带干细胞 (hPDLSCs) 免受氧化应激. 这种抗氧化剂促进骨质分化,表明牙周再生的潜力.
科学领域:
- 干细胞生物学 干细胞生物学
- 牙周再生医学是牙周再生医学.
- 氧化应激研究研究 氧化应激研究
背景情况:
- 牙周炎的发病包括氧化应激,损害人类牙周带干细胞 (hPDLSC) 的再生能力.
- 作为一种强有力的抗氧化剂,阿斯丁 (ASX) 清除活性氧物种 (ROS),但其在氧化应激下对hPDLSCs的影响还未得到充分研究.
研究的目的:
- 研究阿斯丁 (ASX) 对人类牙周带干细胞 (hPDLSCs) 对过氧化 (H2O2) 诱导的氧化应激的保护作用.
- 阐明潜在的机制,包括Nrf2/ARE通路激活和对骨质生分化的影响.
主要方法:
- 分离和鉴定hPDLSCs的特征.
- 通过使用H2O2.2.诱导了氧化应激模型.
- 细胞用ASX进行治疗,评估包括活力,ROS水平,炎症标志物,骨质生成差异化和Nrf2/ARE通路激活.
主要成果:
- ASX显著降低了细胞内和线粒体ROS水平,并保留了线粒体膜潜力.
- ASX抑制了促炎性细胞因子 (TNF-α,IL-1β,IL-6,MCP-1) 的表达.
- ASX促进了骨质分化,并激活了Nrf2/ARE通路,增加了抗氧化酶表达.
结论:
- 阿斯塔丁通过Nrf2/ARE通路改善hPDLSCs中氧化应激诱导的损伤.
- ASX对hPDLSCs表现出抗氧化,抗炎和亲骨质效应.
- 在氧化环境下,ASX对牙周再生具有治疗潜力.
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