机构地区:[1]Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan 430060, China [2]Department of Plastic Surgery, The Third Hospital of Wuhan, Wuhan 430060, China
出 处:《Acta Pharmacologica Sinica》2008年第11期1350-1356,共7页中国药理学报(英文版)
摘 要:Aim: To investigate the effects of resveratrol on interleukin-lbeta (IL-1β) induced catabolism in bone marrow mesenchymal stem cell (MSC) derived chondrocytes cultured on chitosan-gelatin scaffolds (CGS). Methods: The chondrogenesis of alginate-encapsulated MSCs was evaluated by toluidine blue staining, RT-PCR, and immunostaing. MSC-derived chondrocyte morphology cultured on CGS was evaluated by a scanning electron microscope (SEM) and a laser confocal microscope (LCM). When these cells on CGS were pre-stimulated with IL-1 β or co-treated with IL-1 β and resveratrol in the absence and presence of the specific β1-integrin blocking antibody, collagen type Ⅱ, aggrecan, matrix metalloproteinase-13 (MMP-13) expression, and the translocation of nuclear factor kappaB (NF-κB) were analyzed by Western blot analysis. Results: Transforming growth factor beta 3 (TGF-β3) combined with insulin-like growth factor Ⅰ (IGF-Ⅰ) induced the cartilage-specific collagen type Ⅱ, aggrecan expression and extracellular matrix (ECM) accumulation at the end of a 3-week culture. CGS supported those differentiated chondrocytes' attachment, proliferation, migration, and ECM formation. When those cells cultured on CGS were stimulated with IL-1β alone, collagen type Ⅱ and aggrecan expression was inhibited. However, MMP-13 expression increased. Resveratrol reversed the catabolic effects by reducing the translocation of NF-κB. A specific β1-integrin blocking antibody abrogated the effects of resveratrol on IL-1 β stimulated MSC-derived chondrocytes. Conclusion: These results indicated that resveratrol acts as a NF-κB inhibitor to protect MSC-derived chondrocytes on the CGS from the IL-1β catabolism and these effects are mediated by β1-integrin.Aim: To investigate the effects of resveratrol on interleukin-lbeta (IL-1β) induced catabolism in bone marrow mesenchymal stem cell (MSC) derived chondrocytes cultured on chitosan-gelatin scaffolds (CGS). Methods: The chondrogenesis of alginate-encapsulated MSCs was evaluated by toluidine blue staining, RT-PCR, and immunostaing. MSC-derived chondrocyte morphology cultured on CGS was evaluated by a scanning electron microscope (SEM) and a laser confocal microscope (LCM). When these cells on CGS were pre-stimulated with IL-1 β or co-treated with IL-1 β and resveratrol in the absence and presence of the specific β1-integrin blocking antibody, collagen type Ⅱ, aggrecan, matrix metalloproteinase-13 (MMP-13) expression, and the translocation of nuclear factor kappaB (NF-κB) were analyzed by Western blot analysis. Results: Transforming growth factor beta 3 (TGF-β3) combined with insulin-like growth factor Ⅰ (IGF-Ⅰ) induced the cartilage-specific collagen type Ⅱ, aggrecan expression and extracellular matrix (ECM) accumulation at the end of a 3-week culture. CGS supported those differentiated chondrocytes' attachment, proliferation, migration, and ECM formation. When those cells cultured on CGS were stimulated with IL-1β alone, collagen type Ⅱ and aggrecan expression was inhibited. However, MMP-13 expression increased. Resveratrol reversed the catabolic effects by reducing the translocation of NF-κB. A specific β1-integrin blocking antibody abrogated the effects of resveratrol on IL-1 β stimulated MSC-derived chondrocytes. Conclusion: These results indicated that resveratrol acts as a NF-κB inhibitor to protect MSC-derived chondrocytes on the CGS from the IL-1β catabolism and these effects are mediated by β1-integrin.
关 键 词:mesenchymal stem cells alginate chondrogen-esis IL-1β RESVERATROL Β1-INTEGRIN
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