中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (6): 1332-1338.doi: 10.4103/1673-5374.357915

• 原著:脊髓损伤修复保护与再生 • 上一篇    下一篇

人参皂甙 Rb1可改善脊髓损伤后能量代谢

  

  • 出版日期:2023-06-15 发布日期:2023-01-05
  • 基金资助:
    国家自然科学基金项目(81871556,82072165);辽宁振兴人才计划项目(XLYC1902108)

Ginsenoside Rb1 improves energy metabolism after spinal cord injury

Shan Wen1, 2, Zhi-Ru Zou2, 3, Shuai Cheng1, 2, Hui Guo1, 2, Heng-Shuo Hu1, 2, Fan-Zhuo Zeng1, 2, Xi-Fan Mei1, 2, *   

  1. 1Department of Orthopedics, Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province, China; 2Key Laboratory of Medical Tissue Engineering of Liaoning Province, Jinzhou Medical University, Jinzhou, Liaoning Province, China; 3Pharmacy School, Jinzhou Medical University, Jinzhou, Liaoning Province, China
  • Online:2023-06-15 Published:2023-01-05
  • Contact: Xi-Fan Mei, PhD, meixifan@jzmu.edu.cn.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 81871556, 82072165; and Liaoning Revitalization Talents Program, No. XLYC1902108 (all to XFM).

摘要:

氧化应激引起的线粒体损伤和局灶性缺血缺氧引起的能量缺乏是脊髓损伤的重要恶化因素。既往研究显示,人参皂甙Rb1具有神经营养和神经保护作用,其是否也对脊髓损伤后能量代谢有影响,目前尚不清楚。实验采用人参皂甙Rb1对脊髓损伤小鼠模型以及氧糖剥夺细胞模型进行干预,结果显示,人参皂甙Rb1可显著抑制脊髓损伤小鼠神经元氧化应激,并保护线粒体,促进神经元的代谢重编程,增加糖酵解活性和ATP的产生,促进前角运动神经元存活,并促进后肢运动功能的恢复。由于Sirt3对糖酵解和氧化应激有很好的调节作用,因而以Sirt3抑制剂3-TYP对小鼠和细胞进行干预,可见人参皂甙Rb1的治疗效果被明显抑制。因此认为人参皂甙Rb1是治疗脊髓损伤的潜在药物,且其治疗作用与Sirt3密切相关。

https://orcid.org/0000-0002-4452-8005 (Xi-Fan Mei)

关键词: 脊髓损伤, 代谢重编程, 氧化应激, 线粒体, 人参皂苷Rb1, Sirt3, 氧糖剥夺, 神经保护, 糖酵解, 轴突生长

Abstract: Mitochondrial damage caused by oxidative stress and energy deficiency induced by focal ischemia and hypoxia are important factors that aggravate diseases. Studies have shown that ginsenoside Rb1 has neurotrophic and neuroprotective effects. However, whether it influences energy metabolism after spinal cord injury remains unclear. In this study, we treated mouse and cell models of spinal cord injury with ginsenoside Rb1. We found that ginsenoside Rb1 remarkably inhibited neuronal oxidative stress, protected mitochondria, promoted neuronal metabolic reprogramming, increased glycolytic activity and ATP production, and promoted the survival of motor neurons in the anterior horn and the recovery of motor function in the hind limb. Because sirtuin 3 regulates glycolysis and oxidative stress, mouse and cell models of spinal cord injury were treated with the sirtuin 3 inhibitor 3-TYP. When Sirt3 expression was suppressed, we found that the therapeutic effects of ginsenoside Rb1 on spinal cord injury were remarkably inhibited. Therefore, ginsenoside Rb1 is considered a potential drug for the treatment of spinal cord injury, and its therapeutic effects are closely related to sirtuin 3. 

Key words: axon growth, ginsenoside Rb1, glycolysis, metabolic reprogramming, mitochondrion, neuroprotection, oxidative stress, oxygen and glucose deprivation, Sirt3, spinal cord injury