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<p>Oxidative stress-induced vascular smooth muscle cell (VSMC) apoptosis plays a central role in aortic aneurysm (AA) progression. In this study, we developed N, Ce-codoped carbon dots (N, Ce-CDs, ~ 4.8&#xa0;nm) as an efficient nanozyme to counteract this process. The synthesized N, Ce-CDs exhibited superior •OH radical scavenging capability and excellent biocompatibility. In vitro, N, Ce-CDs showed no cytotoxicity toward MOVAS cells, maintaining over 90% cell viability after 72&#xa0;h exposure. More importantly, they demonstrated a significant protective effect against H₂O₂-induced oxidative damage. The nanozymes alleviated oxidative damage by scavenging intracellular reactive oxygen species (ROS), suppressing lipid peroxidation, and boosting endogenous antioxidant capacity through elevated levels of glutathione (GSH) and enhanced activities of superoxide dismutase (SOD) and catalase (CAT). Furthermore, N,Ce-CDs ‌significantly mitigated H₂O₂-induced damage, recovering ~ 60% of the lost mitochondrial membrane potential (MMP) and reducing the apoptosis rate from 31.97% to 18.52%. These findings highlight the potential of N, Ce-CDs as a multifunctional nanotherapeutic agent that protects VSMCs by integrating antioxidant defense with mitochondrial stabilization, presenting a novel strategy for AA treatment.</p>

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The Protective Effect of N, Ce-doped Carbon Dots Against H2O2-Induced Oxidative Damage in MOVAS Cells

  • 期刊论文

  • 发表日期：

    2026年1月8日

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  • Bo Zhao,
  • Yun Tian,
  • Muchen Yu,
  • Jiaming Han,
  • Zhuo Chen,
  • Jiacheng Zhang,
  • Jiaran Liu,
  • Lina Geng,
  • Yuhua Lei

摘要

Oxidative stress-induced vascular smooth muscle cell (VSMC) apoptosis plays a central role in aortic aneurysm (AA) progression. In this study, we developed N, Ce-codoped carbon dots (N, Ce-CDs, ~ 4.8 nm) as an efficient nanozyme to counteract this process. The synthesized N, Ce-CDs exhibited superior •OH radical scavenging capability and excellent biocompatibility. In vitro, N, Ce-CDs showed no cytotoxicity toward MOVAS cells, maintaining over 90% cell viability after 72 h exposure. More importantly, they demonstrated a significant protective effect against H₂O₂-induced oxidative damage. The nanozymes alleviated oxidative damage by scavenging intracellular reactive oxygen species (ROS), suppressing lipid peroxidation, and boosting endogenous antioxidant capacity through elevated levels of glutathione (GSH) and enhanced activities of superoxide dismutase (SOD) and catalase (CAT). Furthermore, N,Ce-CDs ‌significantly mitigated H₂O₂-induced damage, recovering ~ 60% of the lost mitochondrial membrane potential (MMP) and reducing the apoptosis rate from 31.97% to 18.52%. These findings highlight the potential of N, Ce-CDs as a multifunctional nanotherapeutic agent that protects VSMCs by integrating antioxidant defense with mitochondrial stabilization, presenting a novel strategy for AA treatment.