tailieunhanh - Báo cáo y học: "The PI3K–NF-κB signal transduction pathway is involved in mediating the anti-inflammatory effect of IB-MECA in adjuvant-induced arthritis"

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: The PI3K–NF-κB signal transduction pathway is involved in mediating the anti-inflammatory effect of IB-MECA in adjuvant-induced arthritis. | Available online http content 8 1 R33 Research article The PI3K-NF-KB signal transduction pathway is involved in mediating the anti-inflammatory effect of IB-MECA in adjuvant-induced arthritis Pnina Fishman1 2 Sara Bar-Yehuda1 2 Lea Madi1 Lea Rath-Wolfson3 Avivit Ochaion1 Shira Cohen1 and Ehud Baharav2 1Can-Fite BioPharma Ltd. Kiryat-Matalon Petah-Tikva Israel 2Felsenstein Medical Research Center Rabin Medical Center Sackler Faculty of Medicine Tel-Aviv University Petach-Tikva Israel 3Department of Pathology Rabin Medical Center Sackler Faculty of Medicine Tel-Aviv University Petach-Tikva Israel Corresponding author Pnina Fishman pnina@ Received 5 Jun 2005 Revisions requested 14 Jul 2005 Revisions received 5 Dec 2005 Accepted 15 Dec 2005 Published 13 Jan 2006 Arthritis Research Therapy 2006 8 R33 doi ar1 887 This article is online at http content 8 1 R33 2006 Fishman 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. Open Access Abstract The anti-inflammatory effect of adenosine was previously found to be mediated via activation of the A3 adenosine receptor A3AR . The aim of the present study was to decipher the molecular mechanism involved with the inhibitory effect of IB-MECA an A3AR agonist on adjuvant-induced arthritis. The adjuvant-induced arthritis rats responded to IB-MECA treatment with a decrease in the clinical score and the pathological score of the disease. The response to IB-MECA was neutralized by the antagonist MRS 1220 confirming that the efficacy of the synthetic agonist was A3AR mediated. The A3AR protein expression level was highly expressed in the synovia in the peripheral blood mononuclear cells and in the drain lymph node DLN tissues