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10.1007/s10571-015-0264-9 http://scihub22266oqcxt.onion/10.1007/s10571-015-0264-9 C4894924!4894924!27002719     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Neurobiol 2016 ; 36 (ä): 811-20 Nephropedia Template TP {{tp|p=27002719|t=2016. ?-Mangostin Inhibits ?-Synuclein-Induced Microglial Neuroinflammation and Neurotoxicity |pdf=|usr=}}{{27002719}} gab.com Text -Mangostin Inhibits -Synuclein-Induced Microglial Neuroinflammation and Neurotoxicity JO: Cell Mol Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=27002719 #FOAvip Microglia-mediated neuroinflammation induced by ?-synuclein in the substantianigra likely either initiates or aggravates nigral neuro degeneration in Parkinson?s disease (PD). We aimed to explore the effects of ?-mangostin (?-M), a polyphenolicxanthone derivative from mangosteen on ?-synuclein-stimulated DA neurodegeneration. Primary microglia, mesencephalic neuron, mesencephalic neuron-glianeuronal cultures, and transwell co-cultures were prepared separately. Liquid scintillation counting was used to determine the radioactivity in DA uptake. Enzyme-linked immunosorbent assay (ELISA) was performed in the IL-1?, IL-6, and TNF-? assay. The expression of proteins was analyzed by Western blot. ?-M inhibited the increased levels of pro-inflammatory cytokines, NO, and ROS in ?-synuclein-stimulated primary microglia. Mechanistic study revealed that ?-M functioned by inhibition of nuclear factor kappa B (NF-?B) and NADPH oxidase. Further, ?-M protected ?-synuclein-induced microglial and direct neurotoxicity. Although detailed mechanisms remain to be defined, our observations suggest a potential compound, which inhibits microglial activation induced by ?-synuclein by targeting NADPH oxidase, might be a therapeutic possibility in preventing PD progression. Twit Text FOAVip -Mangostin Inhibits -Synuclein-Induced Microglial Neuroinflammation and Neurotoxicity ????Cell Mol Neurobiol http://www.kidney.de/pget.php?&tw=1&pmid=27002719 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27002719 #FOAvip English Wikipedia <ref>{{Cite pmid|27002719}}</ref> ?-Mangostin Inhibits ?-Synuclein-Induced Microglial Neuroinflammation and Neurotoxicity #MMPMID27002719 Hu Z; Wang W; Ling J; Jiang C Cell Mol Neurobiol 2016[]; 36 (ä): 811-20 PMID27002719show ga Microglia-mediated neuroinflammation induced by ?-synuclein in the substantianigra likely either initiates or aggravates nigral neuro degeneration in Parkinson?s disease (PD). We aimed to explore the effects of ?-mangostin (?-M), a polyphenolicxanthone derivative from mangosteen on ?-synuclein-stimulated DA neurodegeneration. Primary microglia, mesencephalic neuron, mesencephalic neuron-glianeuronal cultures, and transwell co-cultures were prepared separately. Liquid scintillation counting was used to determine the radioactivity in DA uptake. Enzyme-linked immunosorbent assay (ELISA) was performed in the IL-1?, IL-6, and TNF-? assay. The expression of proteins was analyzed by Western blot. ?-M inhibited the increased levels of pro-inflammatory cytokines, NO, and ROS in ?-synuclein-stimulated primary microglia. Mechanistic study revealed that ?-M functioned by inhibition of nuclear factor kappa B (NF-?B) and NADPH oxidase. Further, ?-M protected ?-synuclein-induced microglial and direct neurotoxicity. Although detailed mechanisms remain to be defined, our observations suggest a potential compound, which inhibits microglial activation induced by ?-synuclein by targeting NADPH oxidase, might be a therapeutic possibility in preventing PD progression. ä?-Mangostin Inhibits ?-Synuclein-Induced Microglial Neuroinflammation (epmc).pdf DeepDyve Pubget Overpricing