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P1‐309: Global gene expression analysis of paraquat‐induced changes in BV2 microglia cells
Author(s) -
Jee Seung Wan
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.862
Subject(s) - microglia , gene expression , nitric oxide , paraquat , microbiology and biotechnology , biology , cxcl1 , gene , chemokine , chemistry , inflammation , immunology , biochemistry , endocrinology
protecting beta-amyloid and protecting neurons from beta-amyloid-induced degeneration. Methods: Sandwich Enzyme-Linked ImmunoSorbent Assay (sELISA), Western blot, TUNEL staining and cell culture. Results: We observed that 2-AG significantly reduced production of beta-amyloid in NG108-15 cells transfected with the plasmid containing APPsw. We also found that 2-AG suppressed beta-amyloid-induced elevation of COX-2 in hippocampal neurons in culture through a CB1 receptor-dependent mechanism. To further determine the role of 2-AG in beta-amyloid-induced neurodegeneration, caspase-3, an apoptotic marker, was detected in cultured hippocampal neurons in the presence of beta-amyloid. We demonstrated that 2-AG produced a dose-dependent inhibition of caspase-3. In addition, we observed that 2-AG reduced the number of degenerated neurons in culture treated with beta-amyloid, and this reduction was blocked by SR141716 (SR), a CB1 receptor antagonist. Conclusions: Our results indicate that the protective effects of 2-AG on beta-amyloid-induced neurodegeneration are likely through its suppression of neuroinflammation, suggesting that 2-AG has potential as a new therapeutic approach for preventing, ameliorating or treating neurodegenerative diseases such as Alzheimer’s disease.