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:Apigenin, a non-mutagenic dietary flavonoid, suppresses lupus by inhibiting autoantigen presentation for expansion of autoreactive Th1 and Th17 cells. | Available online http content 11 2 R59 Research article Apigenin a non-mutagenic dietary flavonoid suppresses lupus by inhibiting autoantigen presentation for expansion of autoreactive Th1 and Th17 cells Hee-Kap Kang Diane Ecklund Michael Liu and Syamal K Datta Division of Rheumatology Departments of Medicine and Microbiology-Immunology Northwestern University Feinberg School of Medicine 240 East Huron Street Chicago IL 60611 USA Corresponding author Syamal K Datta skd257@ Received 15 Jan 2009 Revisions requested 4 Mar 2009 Revisions received 26 Mar 2009 Accepted 30 Apr 2009 Published 30 Apr 2009 Arthritis Research Therapy 2009 11 R59 doi ar2682 This article is online at http content 11 2 R59 2009 Kang 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 Introduction Lupus patients need alternatives to steroids and cytotoxic drugs. We recently found that apigenin a non-mutagenic dietary flavonoid can sensitize recurrently activated normal human T cells to apoptosis by inhibiting nuclear factor-kappa-B NF-KB -regulated Bcl-xL cyclooxygenase 2 COX-2 and cellular FLICE-like inhibitory protein c-FLIP expression. Because sustained immune activation and hyperexpression of COX-2 and c-FLIP contribute to lupus we treated SNF1 mice that spontaneously develop human lupus-like disease with apigenin. Methods SNF1 mice with established lupus-like disease were injected with 20 mg kg of apigenin daily and then monitored for development of severe nephritis. Histopathologic changes in kidneys IgG autoantibodies to nuclear autoantigens in serum and in cultures of splenocytes along with nucleosome-specific T helper 1 Th1 and Th17 responses COX-2 .
