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: Effects of short-term glucocorticoid treatment on changes in cartilage matrix degradation and chondrocyte gene expression induced by mechanical injury and inflammatory cytokines. | Lu et al. Arthritis Research Therapy 2011 13 R142 http content 13 5 R142 RESEARCH ARTICLE Open Access Effects of short-term glucocorticoid treatment on changes in cartilage matrix degradation and chondrocyte gene expression induced by mechanical injury and inflammatory cytokines Yihong CS Lu1 Christopher H Evans2 and Alan J Grodzinsky1 3 Abstract Introduction Traumatic joint injury damages cartilage and causes adjacent joint tissues to release inflammatory cytokines increasing the risk of developing osteoarthritis. The main objective of this study was to determine whether the combined catabolic effects of mechanical injury tumor necrosis factor alpha TNFa and interleukin-6 IL-6 soluble IL-6 receptor sIL-6R on cartilage could be abolished by short-term treatment with glucocorticoids such as dexamethasone. Methods In an initial dexamethasone-dose-response study bovine cartilage explants were treated with TNFa and increasing concentrations of dexamethasone. Bovine and human cartilage explants were then subjected to individual and combined treatments with TNFa IL-6 sIL-6R and injury in the presence or absence of dexamethasone. Treatment effects were assessed by measuring glycosaminoglycans GAG release to the medium and synthesis of proteoglycans. Additional experiments tested whether pre-exposure of cartilage to dexamethasone could prevent GAG loss and inhibition of biosynthesis induced by cytokines and whether posttreatment with dexamethasone could diminish the effects of pre-established cytokine insult. Messenger ribonucleic acid mRNA levels for genes involved in cartilage homeostasis proteases matrix molecules cytokines growth and transcription factors were measured in explants subjected to combined treatments with injury TNFa and dexamethasone. To investigate mechanisms associated with dexamethasone regulation of chondrocyte metabolic response glucocorticoid receptor GR antagonist RU486 and proprotein convertase inhibitor RVKR-CMK were used.
