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PBN protects NP cells from AAPH-induced degenerative changes by inhibiting the ERK1/2 pathway

Zhenggang Zhou1, Yini Wang2, Haifei Liu3

  • 1Medical College, Qingdao University, Qingdao, Shandong, China.

Connective Tissue Research
|March 19, 2020
PubMed

Insights

N-tert-butyl-α-phenylnitrone (PBN) protects intervertebral disc cells from oxidative stress and degeneration. This free radical scavenger alleviates matrix degradation and apoptosis, offering a potential therapeutic strategy for intervertebral disc degeneration (IDD).

Area of Science:

  • Biomedical Sciences
  • Cell Biology
  • Biochemistry

Background:

  • Intervertebral disc degeneration (IDD) is a major cause of spinal disorders.
  • Oxidative stress significantly contributes to the pathogenesis of IDD.
  • Antioxidant therapies are promising for treating IDD.

Purpose of the Study:

  • To investigate the protective effects of N-tert-butyl-α-phenylnitrone (PBN) against IDD.
  • To determine if PBN alleviates oxidative stress and pathological changes in intervertebral disc cells.

Main Methods:

  • Nucleus pulposus (NP) cells were isolated from rabbit lumbar discs.
  • MTT assay, real-time PCR, and western blotting were used to assess PBN's effects.
  • Oxidative damage was induced using 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH).

Main Results:

  • AAPH induced oxidative stress, matrix degradation, and apoptosis in NP cells via the ERK/MAPK pathway.
  • PBN significantly ameliorated AAPH-induced oxidative stress and degenerative changes.
  • PBN suppressed AAPH-induced activation of the ERK/MAPK pathway, matrix-degrading proteases, and apoptosis.

Conclusions:

  • PBN demonstrates a novel protective role against oxidative stress, matrix catabolism, and apoptosis in intervertebral discs.
  • The mechanism involves suppressing the ERK/MAPK pathway.
  • PBN holds potential for therapeutic applications in combating IDD.
Keywords:
ERK1/2 signaling pathwayIntervertebral disc degenerationN-tert-butyl-alfa-phenylnitronenucleus pulposus cellsoxidative stress

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