P Behrendt1, A Preusse-Prange2, T Klüter3, M Haake4, B Rolauffs5, A J Grodzinsky6, S Lippross7, B Kurz8. 1. Department of Trauma Surgery, University Medical Center Schleswig-Holstein, Campus Kiel, Germany. Electronic address: peter.behrendt@uksh.de. 2. Institute of Anatomy, Christian Albrechts-University, Kiel, Germany. Electronic address: a.preusse@anat.uni-kiel.de. 3. Department of Trauma Surgery, University Medical Center Schleswig-Holstein, Campus Kiel, Germany. Electronic address: tim.klueter@uksh.de. 4. Institute of Anatomy, Christian Albrechts-University, Kiel, Germany. Electronic address: marina.haake@web.de. 5. Siegfried Weller Institute for Trauma Research & Clinic for Trauma and Restorative Surgery, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany; Department of Orthopedics and Trauma Surgery, Albert Ludwigs University of Freiburg, Freiburg, Germany. Electronic address: brolauffs@bgu-tuebingen.de. 6. Massachusetts Institute of Technology, Cambridge, MA, USA. Electronic address: alg@mit.edu. 7. Department of Trauma Surgery, University Medical Center Schleswig-Holstein, Campus Kiel, Germany. Electronic address: sebastian.lippross@uksh.de. 8. Institute of Anatomy, Christian Albrechts-University, Kiel, Germany. Electronic address: bkurz@anat.uni-kiel.de.
Abstract
OBJECTIVE: The aim of this study was to examine whether anti-inflammatory interleukin-10 (IL-10) exerts chondroprotective effects in an in vitro model of a single mechanical injury of mature articular cartilage. METHOD: Articular cartilage was harvested from the femoro-patellar groove of adult cows (Bos taurus) and cultured w/o bovine IL-10. After 24 h of equilibration explants were subjected to an axial unconfined compression (50% strain, velocity 2 mm/s, held for 10 s). After 96 h cell death was measured histomorphometrically (nuclear blebbing, NB) and the release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analyzed. mRNA levels of matrix degrading enzymes and nitric oxide synthetase were measured by quantitative real time PCR. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test. RESULTS: Injurious compression significantly increased the number of cells with NB, release of GAG and nitric oxide and expression of MMP-3, -13, ADAMTS-4 and NOS2. Administration of IL-10 significantly reduced the injury related cell death and release of GAG and NO, respectively. Expression of MMP-3, -13, ADAMTS-4 and NOS2 were significantly reduced. CONCLUSION: Joint injury is a complex process involving specific mechanical effects on cartilage as well as induction of an inflammatory environment. IL-10 prevented crucial mechanisms of chondrodegeneration induced by an injurious single compression. IL-10 might be a multipurpose drug candidate for the treatment of cartilage-related sports injuries or osteoarthritis (OA).
OBJECTIVE: The aim of this study was to examine whether anti-inflammatory interleukin-10 (IL-10) exerts chondroprotective effects in an in vitro model of a single mechanical injury of mature articular cartilage. METHOD:Articular cartilage was harvested from the femoro-patellar groove of adult cows (Bos taurus) and cultured w/o bovineIL-10. After 24 h of equilibration explants were subjected to an axial unconfined compression (50% strain, velocity 2 mm/s, held for 10 s). After 96 h cell death was measured histomorphometrically (nuclear blebbing, NB) and the release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analyzed. mRNA levels of matrix degrading enzymes and nitric oxide synthetase were measured by quantitative real time PCR. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test. RESULTS: Injurious compression significantly increased the number of cells with NB, release of GAG and nitric oxide and expression of MMP-3, -13, ADAMTS-4 and NOS2. Administration of IL-10 significantly reduced the injury related cell death and release of GAG and NO, respectively. Expression of MMP-3, -13, ADAMTS-4 and NOS2 were significantly reduced. CONCLUSION: Joint injury is a complex process involving specific mechanical effects on cartilage as well as induction of an inflammatory environment. IL-10 prevented crucial mechanisms of chondrodegeneration induced by an injurious single compression. IL-10 might be a multipurpose drug candidate for the treatment of cartilage-related sports injuries or osteoarthritis (OA).
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