Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Modulation of LPS stimulated NF-kappaB mediated Nitric . | Journal of Inflammation BioMed Central Research Modulation of LPS stimulated NF-kappaB mediated Nitric Oxide production by PKCe and JAK2 in RAW macrophages Edward Jones1 Ian M Adcock2 Bushra Y Ahmed1 and Neville A Punchard 3 Open Access Address division of Science University of Luton Luton. UK 2Airway Diseases NHLI Imperial College London London. UK and 3School of Health Biosciences University of East London London. UK Email Edward Jones - edward_r_jones@ Ian M Adcock - BushraY Ahmed - Neville A Punchard - Corresponding author Published 24 November 2007 Received 16 April 2007 Accepted 24 November 2007 Journal of Inflammation 2007 4 23 doi 1476-9255-4-23 This article is available from http content 4 1 23 2007 Jones 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 Background Nuclear factor kappa B NF-kB has been shown to play an important role in regulating the expression of many genes involved in cell survival immunity and in the inflammatory processes. NF-kB activation upregulates inducible nitric oxide synthase leading to enhanced nitric oxide production during an inflammatory response. NF-kB activation is regulated by distinct kinase pathways independent of inhibitor of kB kinase IKK . Here we examine the role of protein kinase C isoforms and janus activated kinase 2 JAK2 activation in NF-kB activation and LPS-stimulated NO production. Methods Murine RAW macrophages were treated with lipopolysaccharide LPS Phorbol 12-myristate 13-acetate PMA and a combination of LPS and PMA in the presence or absence of various inhibitors of PKC isoforms and JAK2. Nuclear translocation of the NF-kB .