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: Neuronal oxidative damage and dendritic degeneration following activation of CD14-dependent innate immune response in vivo | Journal of Neuroinflammation BioMed Central Review Open Access Neuronal oxidative damage and dendritic degeneration following activation of CD14-dependent innate immune response in vivo Dejan Milatovic Snjezana Zaja-Milatovic Kathleen S Montine Feng-Shiun Shie and Thomas J Montine Address Department of Pathology University of Washington Harborview Medical Center Seattle Washington 98104 USA Email Dejan Milatovic - dejanm@ Snjezana Zaja-Milatovic - szm@ Kathleen S Montine - kmontine@ Feng-Shiun Shie - fshie@ Thomas J Montine - tmontine@ Corresponding author Published 21 October 2004 Received 6 October 2004 Journal of Neuroinflammation 2004 1 20 doi 1742-2094-1-20 Accepted 21 October 2004 This article is available from http content 1 1 20 2004 Milatovic 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 The cause-and-effect relationship between innate immune activation and neurodegeneration has been difficult to prove in complex animal models and patients. Here we review findings from a model of direct innate immune activation via CD 14 stimulation using intracerebroventricular injection of lipopolysaccharide. These data show that CD14-dependent innate immune activation in cerebrum leads to the closely linked outcomes of neuronal membrane oxidative damage and dendritic degeneration. Both forms of neuronal damage could be blocked by ibuprofen and alphatocopherol but not naproxen or gamma-tocopherol at pharmacologically relevant concentrations. This model provides a convenient method to determine effective agents and their appropriate dose ranges for protecting neurons from CD14-activated innate .
