Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Adiponectin is a potential catabolic mediator in osteoarthritis cartilage. | Kang et al. Arthritis Research Therapy 2010 12 R231 http content 12 6 R231 RESEARCH ARTICLE Open Access Adiponectin is a potential catabolic mediator in osteoarthritis cartilage Eun Ha Kang 1 Yun Jong Lee1 2 Tae Kyun Kim3 Chong Bum Chang3 Jin-Haeng Chung4 Kichul Shin5 Eun Young Lee2 5 Eun Bong Lee2 5 Yeong Wook Song2 5 Abstract Introduction Adiponectin has been implicated in the pathogenesis of osteoarthritis OA . We studied the effects of adiponectin on the OA cartilage homeostasis. Methods Immunohistochemical analysis was performed to evaluate differential expression of adiponectin receptors AdipoRs in nonlesional and lesional areas of OA cartilage. Cartilage and chondrocytes from the knee joints of primary OA patients were cultured in the presence of adiponectin 0 30 gg ml . The levels of total nitric oxide NO matrix metalloproteinase MMP -1 -3 and -13 and tissue inhibitor of metalloproteinase TIMP -1 were measured in the conditioned media. The levels of inducible NO synthase iNOS and MMPs were determined with the quantitative real-time reverse transcription-polymerase chain reaction. The concentrations of collagenase-cleaved type II collagen neoepitope C1-2C were determined in the supernatant of adiponectin-stimulated OA cartilage explants. The effects of kinase and NOS inhibitors were evaluated in the adiponectin-stimulated chondrocytes. Results The expression levels of both AdipoR1 and AdipoR2 were significantly higher in lesional than in nonlesional areas of OA cartilage. The increased rate of AdipoR1-positive chondrocytes was twice that of AdipoR2-positive chondrocytes when compared between nonlesional and lesional areas. Adiponectin-stimulated OA chondrocytes showed increased total NO and MMP-1 -3 and -13 levels compared with nonstimulated cells. The TIMP-1 level was not affected. The C1-2C levels were increased by adiponectin in OA cartilage explant culture. AMP-activated protein kinase AMPK and c-Jun N-terminal kinase JNK .
