Diosgenin Glucoside Protects against Spinal Cord Injury by Regulating Autophagy and Alleviating Apoptosis

DOI Web Site 被引用文献1件
  • Xian-Bing Chen
    West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China
  • Zi-Li Wang
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Qing-Yu Yang
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Fang-Yu Zhao
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Xiao-Li Qin
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Xian-E Tang
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Jun-Long Du
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Zong-Hai Chen
    College of Medicine, Hubei University for Nationalities, Enshi 445000, China
  • Kui Zhang
    West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China
  • Fei-Jun Huang
    West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu 610041, China

説明

<jats:p>Spinal cord injury (SCI) is a severe traumatic lesion of central nervous system (CNS) with only a limited number of restorative therapeutic options. Diosgenin glucoside (DG), a major bioactive ingredient of Trillium tschonoskii Max., possesses neuroprotective effects through its antioxidant and anti-apoptotic functions. In this study, we investigated the therapeutic benefit and underlying mechanisms of DG treatment in SCI. We found that in Sprague-Dawley rats with traumatic SCI, the expressions of autophagy marker Light Chain 3 (LC3) and Beclin1 were decreased with concomitant accumulation of autophagy substrate protein p62 and ubiquitinated proteins, indicating an impaired autophagic activity. DG treatment, however, significantly attenuated p62 expression and upregulated the Rheb/mTOR signaling pathway (evidenced as Ras homolog enriched in brain) due to the downregulation of miR-155-3p. We also observed significantly less tissue injury and edema in the DG-treated group, leading to appreciable functional recovery compared to that of the control group. Overall, the observed neuroprotection afforded by DG treatment warrants further investigation on its therapeutic potential in SCI.</jats:p>

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