Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Activation of microglial NADPH oxidase is synergistic with glial iNOS expression in inducing neuronal death: a dual-key mechanism of inflammatory neurodegeneration | Journal of Neuroinflammation BioMed Central Research Open Access Activation of microglial NADPH oxidase is synergistic with glial iNOS expression in inducing neuronal death a dual-key mechanism of inflammatory neurodegeneration Palwinder Mander and Guy C Brown Address Biochemistry Department University of Cambridge Tennis Court Road Cambridge CB2 1QW UK Email Palwinder Mander - pkm22@ Guy C Brown - gcb@ Corresponding author Published 12 September 2005 Received 25 July 2005 Journal ofNeuroinflammation 2005 2 20 doi 1742-2094-2-20 Accepted 12 September 2005 This article is available from http content 2 1 20 2005 Mander and Brown 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 Inflammation-activated glia are seen in many CNS pathologies and may kill neurons through the release of cytotoxic mediators such as nitric oxide from inducible NO synthase iNOS and possibly superoxide from NADPH oxidase NOX . We set out to determine the relative role of these species in inducing neuronal death and to test the dual-key hypothesis that the production of both species simultaneously is required for significant neuronal death. Methods Primary co-cultures of cerebellar granule neurons and glia from rats were used to investigate the effect of NO from iNOS following lipopolysaccharide LPS and or cytokine addition or superoxide hydrogen peroxide from NOX following phorbol 12-myristate 13-acetate PMA ATP analogue BzATP interleukin-1 p IL-1 P or arachidonic acid AA addition on neuronal survival. Results Induction of glial iNOS caused little neuronal death. Similarly activation of NOX alone resulted in little or no neuronal death. However if NOX was activated by PMA .
