<p>Intervertebral disc degeneration (IDD) is characterized by the abnormal synthesis of extracellular matrix (ECM) proteins, increased inflammatory cytokines, and upregulated degradative enzymes. According to the Traditional Chinese Medicine (TCM) concept, the degenerative disease of the intervertebral disc falls under the heading of “stagnation syndrome.” Bu-Shen-Huo-Xue-Fang (BSHXF) is commonly applied to the treatment of IDD. In the present study, IDD models were established in rats, and degeneration, including morphological and histopathological alterations, the loss of collagen and proteoglycan, and increased MMP-13 and ADAMTS-5 were observed. BSHXF significantly ameliorated these degenerative alterations, decreased pro-inflammatory factors, and inhibited NF-κB signaling activation. Aucubin and Tanshinol were identified as the two main active ingredients of BSHXF. In IDD rats, Aucubin or Tanshinol treatment also remarkably relieved degenerative alterations. Moreover, Aucubin or Tanshinol treatment reduced IL-1β, TNF-α, P16, and P19 mRNA and protein expression, suppressed p65 phosphorylation, and decreased β-catenin protein contents within IDD samples. In conclusion, BSHXF, Aucubin, or Tanshinol improves IDD through affecting nucleus pulposus (NP) cell senescence and ECM metabolism; the Wnt/β-catenin and NF-κB signaling might contribute to the BSHXF, Aucubin, or Tanshinol process, ameliorating IDD.</p>

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Aucubin and Tanshinol from Bu-Shen-Huo-Xue-Fang (BSHXF) improve intervertebral disc degeneration through affecting nucleus pulposus cell

  • Linghui Li,
  • Xitong Yan,
  • Liming Zheng,
  • Xu Wei,
  • Shangquan Wang,
  • Xin Chen,
  • Kaiming Li,
  • Xunlu Yin,
  • Minshan Feng

摘要

Intervertebral disc degeneration (IDD) is characterized by the abnormal synthesis of extracellular matrix (ECM) proteins, increased inflammatory cytokines, and upregulated degradative enzymes. According to the Traditional Chinese Medicine (TCM) concept, the degenerative disease of the intervertebral disc falls under the heading of “stagnation syndrome.” Bu-Shen-Huo-Xue-Fang (BSHXF) is commonly applied to the treatment of IDD. In the present study, IDD models were established in rats, and degeneration, including morphological and histopathological alterations, the loss of collagen and proteoglycan, and increased MMP-13 and ADAMTS-5 were observed. BSHXF significantly ameliorated these degenerative alterations, decreased pro-inflammatory factors, and inhibited NF-κB signaling activation. Aucubin and Tanshinol were identified as the two main active ingredients of BSHXF. In IDD rats, Aucubin or Tanshinol treatment also remarkably relieved degenerative alterations. Moreover, Aucubin or Tanshinol treatment reduced IL-1β, TNF-α, P16, and P19 mRNA and protein expression, suppressed p65 phosphorylation, and decreased β-catenin protein contents within IDD samples. In conclusion, BSHXF, Aucubin, or Tanshinol improves IDD through affecting nucleus pulposus (NP) cell senescence and ECM metabolism; the Wnt/β-catenin and NF-κB signaling might contribute to the BSHXF, Aucubin, or Tanshinol process, ameliorating IDD.