báo cáo hóa học: "Fibrillar beta-amyloid peptide Aβ1–40 activates microglial proliferation via stimulating TNF-α release and H2O2 derived from NADPH oxidase: a cell culture study"

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: Fibrillar beta-amyloid peptide Aβ1–40 activates microglial proliferation via stimulating TNF-α release and H2O2 derived from NADPH oxidase: a cell culture study | Journal of Neuroinflammation BioMed Central Research Open Access Fibrillar beta-amyloid peptide Ap1-40 activates microglial proliferation via stimulating TNF-a release and H2O2 derived from NADPH oxidase a cell culture study Aiste Jekabsone1 Palwinder K Mander1 Anna Tickler2 Martyn Sharpe3 and Guy C Brown 1 Address Department of Biochemistry University of Cambridge Tennis Court Road Cambridge CB2 1QW UK 2Cavendish laboratory University of Cambridge Cambridge CB3 0HE UK and 3Biochemistry and Molecular Biology Department Biochemistry Building Michigan State University East Lansing MI 48824-1319 USA Email Aiste Jekabsone - aj293@ Palwinder K Mander - Anna Tickler - annatickler@ Martyn Sharpe - msharpe@ Guy C Brown - gcb@ Corresponding author Published 07 September 2006 Received 16 March 2006 Accepted 07 September 2006 Journal of Neuroinflammation 2006 3 24 doi 1742-2094-3-24 This article is available from http content 3 1 24 2006 Jekabsone 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 Alzheimer s disease is characterized by the accumulation of neuritic plaques containing activated microglia and p-amyloid peptides AP . Fibrillar Ap can activate microglia resulting in production of toxic and inflammatory mediators like hydrogen peroxide nitric oxide and cytokines. We have recently found that microglial proliferation is regulated by hydrogen peroxide derived from NADPH oxidase. Thus in this study we investigated whether Ap can stimulate microglial proliferation and cytokine production via activation of NADPH oxidase to produce hydrogen peroxide. Methods Primary mixed glial cultures were

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