title: Anti-inflammatory and anti-catabolic effects of TENDOACTIVE® on human tenocytes in vitro.
abstract: 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.
authors.affiliation: Musculoskeletal Research Group, Institute of Anatomy, Ludwig-Maximilian-University Munich, Munich, Germany. mehdi.shakibaei@med.uni-muenchen.de
authors.forename: M
authors.initials: M
authors.lastname: Shakibaei
authors.forename: C
authors.initials: C
authors.lastname: Buhrmann
authors.forename: A
authors.initials: A
authors.lastname: Mobasheri
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002467:Cell Nucleus / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002469:Cell Separation; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects; D003470:Culture Media; D019587:Dietary Supplements; D005455:Fluorescent Antibody Technique; D006801:Humans; D053583:Interleukin-1beta / Q000502:physiology; D008297:Male; D008660:Metabolism / Q000187:drug effects*; D046529:Microscopy, Electron, Transmission; D008875:Middle Aged; D008928:Mitochondria / Q000187:drug effects; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics; D015398:Signal Transduction / Q000187:drug effects; D013710:Tendons / Q000166:cytology* / Q000187:drug effects*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D003470:Culture Media; D053583:Interleukin-1beta; D016328:NF-kappa B; D051996:Transcription Factor RelA