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<p>Mitochondrial oxidative stress is an important factor affecting the biological activity of stem cells under degenerative microenvironments. Cartilage endplate–derived stem cells (CESCs) are considered to participate in intervertebral disc homeostasis; however, their mitochondrial redox status under degeneration-related conditions remains incompletely characterized. In this study, human CESCs were isolated from patients with different degrees of intervertebral disc degeneration and used as an in vitro model to investigate mitochondrial oxidative stress. For intervention experiments, CESCs were treated with 100 µM melatonin for 24&#xa0;h. Intracellular reactive oxygen species and mitochondrial superoxide were assessed using DCFH-DA and MitoSO™ Red, respectively. Mitochondrial membrane potential, ATP production, catalase and superoxide dismutase activities, and mitochondrial ultrastructure were evaluated. SIRT3 mRNA and protein expression were examined by quantitative real-time PCR and western blotting, and siRNA-mediated SIRT3 knockdown was used to explore its potential involvement in mitochondrial regulation. CESCs derived from advanced degeneration exhibited increased oxidative stress, decreased mitochondrial membrane potential, reduced ATP production, lower antioxidant enzyme activity, and greater mitochondrial ultrastructural damage. Melatonin treatment reduced intracellular ROS and mitochondrial superoxide accumulation and improved mitochondrial function. SIRT3 knockdown reduced SIRT3 mRNA and protein expression and partially attenuated the protective effects associated with melatonin. Melatonin increased SIRT3 mRNA expression, while SIRT3 protein expression was higher in the melatonin-treated group than in the SIRT3-siRNA group. These findings suggest that melatonin improves mitochondrial redox balance and mitochondrial function in human CESCs and that SIRT3 may participate in this regulatory process. The present study provides experimental evidence supporting a potential role for melatonin in modulating mitochondrial oxidative stress under degeneration-associated conditions.</p>

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Melatonin improves mitochondrial function and redox balance in human cartilage endplate–derived stem cells

  • 期刊论文

  • 发表日期：

    2026年7月14日

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  • Pingfan Mo,
  • Rongchun Chen,
  • Linbo Sun,
  • Yunsheng Chen,
  • Jun Xiong,
  • Yaohong Wu,
  • Canhua Xu

摘要

Mitochondrial oxidative stress is an important factor affecting the biological activity of stem cells under degenerative microenvironments. Cartilage endplate–derived stem cells (CESCs) are considered to participate in intervertebral disc homeostasis; however, their mitochondrial redox status under degeneration-related conditions remains incompletely characterized. In this study, human CESCs were isolated from patients with different degrees of intervertebral disc degeneration and used as an in vitro model to investigate mitochondrial oxidative stress. For intervention experiments, CESCs were treated with 100 µM melatonin for 24 h. Intracellular reactive oxygen species and mitochondrial superoxide were assessed using DCFH-DA and MitoSO™ Red, respectively. Mitochondrial membrane potential, ATP production, catalase and superoxide dismutase activities, and mitochondrial ultrastructure were evaluated. SIRT3 mRNA and protein expression were examined by quantitative real-time PCR and western blotting, and siRNA-mediated SIRT3 knockdown was used to explore its potential involvement in mitochondrial regulation. CESCs derived from advanced degeneration exhibited increased oxidative stress, decreased mitochondrial membrane potential, reduced ATP production, lower antioxidant enzyme activity, and greater mitochondrial ultrastructural damage. Melatonin treatment reduced intracellular ROS and mitochondrial superoxide accumulation and improved mitochondrial function. SIRT3 knockdown reduced SIRT3 mRNA and protein expression and partially attenuated the protective effects associated with melatonin. Melatonin increased SIRT3 mRNA expression, while SIRT3 protein expression was higher in the melatonin-treated group than in the SIRT3-siRNA group. These findings suggest that melatonin improves mitochondrial redox balance and mitochondrial function in human CESCs and that SIRT3 may participate in this regulatory process. The present study provides experimental evidence supporting a potential role for melatonin in modulating mitochondrial oxidative stress under degeneration-associated conditions.