intravenous administration of anti-vascular endothelial growth factor humanized monoclonal antibody bevacizumab improves articular cartilage repair静脉anti-vascular内皮生长因子管理人性化单克隆抗体贝伐单抗改善关节软骨修复.pdfVIP

intravenous administration of anti-vascular endothelial growth factor humanized monoclonal antibody bevacizumab improves articular cartilage repair静脉anti-vascular内皮生长因子管理人性化单克隆抗体贝伐单抗改善关节软骨修复.pdf

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intravenous administration of anti-vascular endothelial growth factor humanized monoclonal antibody bevacizumab improves articular cartilage repair静脉anti-vascular内皮生长因子管理人性化单克隆抗体贝伐单抗改善关节软骨修复

Nagai et al. Arthritis Research Therapy 2010, 12:R178 /content/12/5/R178 RESEARCH ARTICLE Open Access Intravenous administration of anti-vascular endothelial growth factor humanized monoclonal antibody bevacizumab improves articular cartilage repair * Toshihiro Nagai, Masato Sato , Toshiharu Kutsuna, Mami Kokubo, Goro Ebihara, Naoshi Ohta, Joji Mochida Abstract Introduction: In this study, we investigate the efficacy of repairing an osteochondral defect in rabbit knee joints by administering bevacizumab, a humanized monoclonal anti-vascular endothelial growth factor (VEGF) antibody. Methods: An osteochondral defect was created on the patellar groove of 20 Japanese white rabbits that were classified into two recipient groups: group B, administration of bevacizumab (100-mg intravenous injection on the day of surgery and 2 weeks later), and a control group (defect only). Rabbits were killed 1 and 3 months postoperatively. Sections were stained with safranin O. Repair sites were evaluated using the modified O’Driscoll International Cartilage Repair Society grading system. The expression of chondromodulin (ChM)-I and VEGF was evaluated using immunohistochemical analyses. Results: At 1 month postoperatively, the repair site in group B was filled with cartilaginous tissue. At 3 months, the repair site retained this cartilage phenotype. At 1 month in the controls, the defects were mainly filled with fibrous tissue. At 3 months, the defect was replaced by fibrous tissue and bone. Over the 3-month period, histological scores were significantly higher in group B than in the controls. At 1 month, group B showed intense positive results for ChM-I in the bottom of the repair tissue. VEGF was also identified in the same area. In the controls, no ChM-I was observed in the repair tissue. Con

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