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: Alterations of metabolic activity in human osteoarthritic osteoblasts by lipid . | Available online http content 8 6 R159 Research article Alterations of metabolic activity in human osteoarthritic osteoblasts by lipid peroxidation end product 4-hydroxynonenal Qin Shi France Vaillancourt Véronique Côté Hassan Fahmi Patrick Lavigne Hassan Afif John A Di Battista Julio C Fernandes and Mohamed Benderdour Open Access Orthopaedic Research Laboratory Sacre-Coeur Hospital University of Montreal 5400 Gouin West Montreal Quebec Canada H4J 1 C5 Corresponding author Mohamed Benderdour Received 26 Apr 2006 Revisions requested 13 Jun 2006 Revisions received 13 Sep 2006 Accepted 16 Oct 2006 Published 16 Oct 2006 Arthritis Research Therapy 2006 8 R159 doi ar2066 This article is online at http content 8 6 R159 2006 Shi et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract 4-Hydroxynonenal HNE a lipid peroxidation end product is produced abundantly in osteoarthritic OA articular tissues but its role in bone metabolism is ill-defined. In this study we tested the hypothesis that alterations in OA osteoblast metabolism are attributed in part to increased levels of HNE. Our data showed that HNE protein adduct levels were higher in OA osteoblasts compared to normal and when OA osteoblasts were treated with H2O2. Investigating osteoblast markers we found that HNE increased osteocalcin and type I collagen synthesis but inhibited alkaline phosphatase activity. We next examined the effects of HNE on the signaling pathways controlling cyclooxygenase-2 COX-2 and interleukin-6 IL-6 expression in view of their putative role in OA pathophysiology. HNE dose-dependently decreased basal and tumour necrosis factor-a TNF-a -induced IL-6 expression
