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 α7 nicotinic acetylcholine receptor by nicotine selectively up-regulates cyclooxygenase-2 and prostaglandin E2 in rat microglial cultures | Journal of Neuroinflammation BioMed Central Research Open Access Activation of a7 nicotinic acetylcholine receptor by nicotine selectively up-regulates cyclooxygenase-2 and prostaglandin E2 in rat microglial cultures Roberta De Simone Maria Antonietta Ajmone-Cat Daniela Carnevale and Luisa Minghetti Address Department of Cell Biology and Neurosciences Section of Degenerative and Inflammatory Neurological Diseases Istituto Superiore di Sanità Rome Italy Email Roberta De Simone - desimone@ Maria Antonietta Ajmone-Cat - ajcat@ Daniela Carnevale - carneval@ Luisa Minghetti - minghett@ Corresponding author Published 25 January 2005 Received 14 December 2004 Journal ofNeuroinflammation 2005 2 4 doi 1742-2094-2-4 Accepted 25 January 2005 This article is available from http content 2 1 4 2005 De Simone 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 Nicotinic acetylcholine Ach receptors are ligand-gated pentameric ion channels whose main function is to transmit signals for the neurotransmitter Ach in peripheral and central nervous system. However the a7 nicotinic receptor has been recently found in several non-neuronal cells and described as an important regulator of cellular function. Nicotine and ACh have been recently reported to inhibit tumor necrosis factor-a TNF-a production in human macrophages as well as in mouse microglial cultures. In the present study we investigated whether the stimulation of a7 nicotinic receptor by the specific agonist nicotine could affect the functional state of activated microglia by promoting and or inhibiting the release of other important pro-inflammatory and lipid mediator such as prostaglandin E2. Methods .
