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Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
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Pterostilbene Improves Apoptosis, Inflammation, and Autophagy of Osteoarthritis Chondrocytes Through the

Lei Zhou1, Cong Cong Sun1, Fa Juan Shen2

  • 1Department of Hand Surgery, The Second Affiliated Hospital of Shandong First Medical University, Tai'an City, China.

Journal of Biochemical and Molecular Toxicology
|August 8, 2025
PubMed

Insights

Pterostilbene protects against osteoarthritis by inhibiting the (rat sarcoma virus/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase) pathway, reducing chondrocyte injury and inflammation.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown and inflammation.
  • Chondrocyte apoptosis and extracellular matrix degradation are key pathological features of OA.
  • The (rat sarcoma virus/rapidly accelerated fibrosarcoma/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase) (RAS/RAF/MEK/ERK) pathway plays a critical role in OA pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic effects of pterostilbene on chondrocyte injury in OA.
  • To elucidate the underlying molecular mechanisms, specifically the regulation of the RAS/RAF/MEK/ERK pathway by pterostilbene.

Main Methods:

  • Established OA animal models and cultured interleukin-1β-treated chondrocytes.
  • Administered pterostilbene to in vivo and in vitro models.
  • Assessed cartilage damage, chondrocyte viability, apoptosis, and autophagosome formation.
  • Measured inflammatory factors and key proteins in the RAS/RAF/MEK/ERK pathway using ELISA and Western blot/RT-PCR.

Main Results:

  • Pterostilbene attenuated cartilage injury, improved cartilage morphology, and reduced inflammatory factors in OA mice.
  • Pterostilbene decreased interleukin-1β-induced chondrocyte injury, enhanced viability, reduced apoptosis, and promoted autophagy.
  • Pterostilbene inhibited the expression of MMP-1, MMP-13, cleaved caspase-3, p-p65, and p62, while promoting autophagy-related gene 5 expression.
  • Pterostilbene effectively blocked RAS/RAF/MEK/ERK pathway activation.

Conclusions:

  • Pterostilbene demonstrates significant chondroprotective effects in OA.
  • The therapeutic mechanism involves the inhibition of the RAS/RAF/MEK/ERK pathway.
  • Pterostilbene holds potential as a therapeutic agent for osteoarthritis treatment.
Keywords:
Ras/Raf/MEK/ERK pathwaychondrocyteinflammationosteoarthritispterostilbene

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