TAILIEUCHUNG - báo cáo hóa học: " The acute inflammatory response to intranigral a-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation"

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: The acute inflammatory response to intranigral a-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation | Couch et al. Journal of Neuroinflammation 2011 8 166 http content 8 1 166 JJOURNAL OF. NEUROINFLAMMATION RESEARCH Open Access The acute inflammatory response to intranigral a-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation Yvonne Couch1 Lydia Alvarez-Erviti2 Nicola R Sibson3 Matthew JA Wood4 and Daniel C Anthony1 Abstract Background Activated microglia are a feature of the host response to neurodegeneration in Parkinson s disease PD and are thought to contribute to disease progression. Recent evidence suggests that extracellular a-synuclein eSNCA may play an important role in the pathogenesis of PD and that this may be mediated by a microglial response. Methods We wished to discover whether the host response to eSNCA would be sufficient to induce significant cytokine production. In vitro cultured BV-2 microglia were used to determine the basic inflammatory response to eSNCA. In vivo 8-week old Biozzi mice were subjected to a single intranigral injection of either 3 pg SNCA lipopolysaccharide LPS or serum protein BSA and allowed to recover for 24 hours. A second cohort of animals were peripherally challenged with LPS mg kg 6 hours prior to tissue collection. Inflammation was studied by quantitative real-time PCR for a number of pro-inflammatory genes and immunohistochemistry for microglial activation endothelial activation and cell death. Results In vitro data showed a robust microglial response to SNCA including a positive NFkB response and the production of pro-inflammatory cytokines. Direct injection of SNCA into the substantia nigra resulted in the upregulation of mRNA expression of proinflammatory cytokines the expression of endothelial markers of inflammation and microglial activation. However these results were significantly different to those obtained after direct injection of LPS. By contrast when the animals were injected intracerebrally with SNCA and .

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