Polyphyllin I Mitigated IL-1β-Induced Chondrocytes Damage through Downregulating TWIST1 Expression

Feng Liu1, Bowen Han2, Deshun Yang1

  • 1Department of Orthopedics, Nanjing Pukou District Traditional Chinese Medicine Hospital, Nanjing City, Jiangsu Province, 211800, China.

PubMed
Abstract

Insights

Polyphyllin I (PPI) reduces osteoarthritis (OA) progression by suppressing chondrocyte apoptosis, senescence, and inflammation. PPI achieves this by downregulating TWIST1 expression, offering a potential therapeutic avenue for OA treatment.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage breakdown.
  • Polyphyllin I (PPI) exhibits anti-inflammatory properties, but its mechanism in OA is not fully understood.

Purpose of the Study:

  • To investigate the mechanism of Polyphyllin I (PPI) in osteoarthritis (OA) chondrocytes.
  • To determine the effect of PPI on IL-1β-induced chondrocyte apoptosis, senescence, inflammation, and extracellular matrix (ECM) degradation.

Main Methods:

  • Chondrocytes were treated with IL-1β and varying concentrations of PPI.
  • Cell viability, apoptosis, senescence, and inflammatory factor release were assessed using MTT, flow cytometry, SA-β-Gal assay, and ELISA.
  • Gene and protein expression related to apoptosis, ECM, and TWIST1 were analyzed by qRT-PCR and western blot, with experiments repeated after TWIST1 overexpression.

Main Results:

  • IL-1β reduced chondrocyte count and collagen II density.
  • PPI dose-dependently inhibited IL-1β-induced apoptosis, senescence, and release of IL-6 and TNF-α.
  • PPI decreased cleaved caspase-3, bax, MMP-3, and MMP-13 expression while increasing collagen II expression.
  • PPI downregulated TWIST1 expression, and TWIST1 overexpression reversed these protective effects.

Conclusions:

  • Polyphyllin I (PPI) mitigates apoptosis, senescence, inflammation, and ECM degradation in OA chondrocytes.
  • PPI exerts its protective effects by downregulating TWIST1 expression.
  • TWIST1 is a key mediator in the therapeutic action of PPI against OA progression.

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