Anti-inflammatory and anti-catabolic effects of TENDOACTIVE® on human tenocytes in vitro

Histol Histopathol. 2011 Sep;26(9):1173-85. doi: 10.14670/HH-26.1173.


Tendons have a limited capacity for self-repair due to the low density and mitotic activity of tenocytes. Pro-inflammatory cytokines such as interleukin-1β (IL-1β) have been identified as the main initiators of tendinopathies, stimulating inflammation, apoptosis and extracellular matrix (ECM) degradation. The aim of this study was to evaluate the potential of Tendoactive®, a newly developed proprietary nutraceutical formulation that includes mucopolysaccharides, collagen and vitamin C, in an in vitro model of tendon inflammation. The effects of Tendoactive® were studied in primary cultures of human tenocytes treated with IL-1β for up to 72 h. Expression of collagen type I, integrin β1, cyclo-oxygenase-2 (COX-2), caspase-3 and matrix metalloproteinase-1 (MMP-1) was monitored by western blotting. The effects of Tendoactive® on the expression, phosphorylation and nuclear translocation of protein components of the NF-κB system were studied by western blotting and immunofluorescence respectively. Treatment of tenocytes with Tendoactive® suppressed IL-1β-induced NF-κB activation and p65 nuclear translocation. These events correlated with down-regulation of NF-κB targets including COX-2, MMP-1 and activated caspase-3. Tendoactive® also reversed the IL-1β-induced down-regulation of collagen type I and β1-integrin receptor expression. These results indicate that Tendoactive® has nutraceutical potential as an anti-inflammatory agent for treating tendinopathy through suppression of NF-κB mediated IL-1β catabolic signalling pathways in tenocytes.

MeSH terms

  • Adult
  • Anti-Inflammatory Agents, Non-Steroidal*
  • Apoptosis / drug effects
  • Blotting, Western
  • Cell Nucleus / drug effects
  • Cell Proliferation / drug effects
  • Cell Separation
  • Cell Survival / drug effects
  • Cells, Cultured
  • Chondrocytes / drug effects
  • Culture Media
  • Dietary Supplements*
  • Fluorescent Antibody Technique
  • Humans
  • Interleukin-1beta / physiology
  • Male
  • Metabolism / drug effects*
  • Microscopy, Electron, Transmission
  • Middle Aged
  • Mitochondria / drug effects
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / genetics
  • Signal Transduction / drug effects
  • Tendons / cytology*
  • Tendons / drug effects*
  • Transcription Factor RelA / metabolism


  • Anti-Inflammatory Agents, Non-Steroidal
  • Culture Media
  • Interleukin-1beta
  • NF-kappa B
  • Transcription Factor RelA