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: Ginkgolide B inhibits the neurotoxicity of prions or amyloid-β1-42 | Journal of Neuroinflammation BioMed Central Research Open Access Ginkgolide B inhibits the neurotoxicity of prions or Clive Bate 1 Mario Salmona2 and Alun Williams3 Address Department of Veterinary Pathology Glasgow University Veterinary School Bearsden Road Glasgow UK. G61 1QH 2Department of Molecular Biochemistry and Pharmacology Istituto di Ricerche Farmacologiche Mario Negri Via Eritrea 62 20157 Milano Italy and 3Department of Pathology and Infectious Diseases Royal Veterinary College Hawkshead Lane North Mymms Herts UK. AL9 7TA Email Clive Bate - Mario Salmona - salmona@ Alun Williams - alunwilliams@ Corresponding author Published 11 May 2004 Received 08 March 2004 Journal of Neuroinflammation 2004 1 4 Accepted 11 May 2004 This article is available from http content 1 1 4 2004 Bate et al 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 Neuronal loss in Alzheimer s or prion diseases is preceded by the accumulation of fibrillar aggregates of toxic proteins amyloid-P1-42 or the prion protein . Since some epidemiological studies have demonstrated that the EGb 761 extract from the leaves of the Ginkgo biloba tree has a beneficial effect on Alzheimer s disease the effect of some of the major components of the EGb 761 extract on neuronal responses to amyloid-P1-42 or to a synthetic miniprion sPrP106 were investigated. Methods Components of the EGb 761 extract were tested in 2 models of neurodegeneration. SH-SY5Y neuroblastoma cells were pre-treated with ginkgolides A or B quercetin or myricetin and incubated with amyloid-P1-42 sPrP106 or other neurotoxins. After 24 hours neuronal survival and the production of prostaglandin E2 that is closely associated with neuronal death was measured. In
