TAILIEUCHUNG - báo cáo hóa học: " PPARγ, neuroinflammation, and disease"

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: PPARγ, neuroinflammation, and disease | Journal of Neuroinflammation BioMed Central Commentary PPARy neuroinflammation and disease Robert E Mrak 1 and Gary E Landreth2 Open Access Address Department of Pathology University of Arkansas for Medical Sciences Little Rock Arkansas USA and 2Alzheimer Research Laboratory Department of Neurosciences Case Western Reserve University School of Medicine Cleveland Ohio USA Email Robert E Mrak - mrakroberte@ Gary E Landreth - gel2@ Corresponding author Published 14 May 2004 Received 02 April 2004 Accepted 14 May 2004 Journal of Neuroinflammation 2004 1 5 This article is available from http content 1 1 5 2004 Mrak and Landreth licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Background Peroxisome proliferator-activated receptors PPARs are a class of nuclear transcription factors that are activated by fatty acids and their derivatives. One of these PPARy regulates responsiveness to insulin in adipose cells and PPARy-activating drugs such as pioglitazone are used in the treatment of type 2 diabetes. PPARy acts in myeloid-lineage cells including T-cells and macrophages to suppress their activation and their elaboration of inflammatory molecules. PPARy activation also suppresses the activated phenotype in microglia suggesting that PPARy-activating drugs may be of benefit in chronic neuroinflammatory diseases. Some but not all nonsteroidal anti-inflammatory agents indomethacin and ibuprofen in particular also have activating effects on PPARy. Discussion and conclusions These observations suggest on the one hand a role for PPARy-activating drugs in the treatment of chronic neuroinflammatory diseases-as shown for a patient with secondary progressive multiple sclerosis by Pershadsingh et al. in this issue of the Journal of Neuroinflammation-and .

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