PC12 cells exposed to MPP+ (500 mu M) elicited phosphorylation of MKK7, c-Jun-NH2-terminal kinase (JNK), and c-Jun which followed by the increase in cytochrome c levels, and which was prevented by puerarin. Moreover, puerarin inhibited the activation of caspase-9 and caspase-3 in MPP+-exposed PC12 cells. Whereas, the neuroprotective effect of puerarin against MPP+ insults can be blocked by SP600125 (inhibitor of JNK). Taken together, these results suggest

that puerarin protected PC12 cells against MPP+-induced neurotoxicity through the inhibition of the INK signaling pathways. AZD5363 concentration Therefore, puerarin has the possible beneficial effects in PD by attenuating MPP+-induced toxicity. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Endothelial cell tropism is an Inherent property of Isolates of human cytomegalovirus (HCMV), and has been proposed as a pathogenicity factor of HCMV Mutational approaches can be applied for analysis of the molecular determinants of endothelial cell tropism, but the evaluation of mutants is limited by the low reliability of the widely employed cell tropism assay. The aim of this study was to Improve the assay conditions in order to allow for accurate discrimination of

phenotypic differences between Entrectinib HCMV mutants Target cell density and input virus titres were identified to account for most of the variation in the apparent endothelial cell tropism of a given cytomegalovirus strain Coating of culture dishes, cell attachment at ambient temperature, and standardization of virus 3 Methyladenine Input titres together with automated counting of immunofluorescence signals enabled the discrimination of differences of as little as 25% in endothelial cell tropism of HCMV strains This improvement will facilitate rapid and reliable quantitation of cell tropism of HCMV, and is particularly suitable for the analysis of large numbers of mutants with only minor changes in tropism (C) 2010 Elsevier B V All rights reserved”
“A mouse and human brain-enriched micro-RNA-146a (miRNA-146a) is known

to be important in modulating the innate immune response and inflammatory signaling in certain immunological and brain cell types. In this study we examined miRNA-146a levels in early-, moderate- and late-stage Alzheimer’s disease (AD) neocortex and hippocampus, in several human primary brain and retinal cell lines, and in 5 different transgenic mouse models of AD including Tg2576, TgCRND8, PSAPP, 3xTg-AD and 5xFAD. Inducible expression of miRNA-146a was found to be significantly up-regulated in a primary co-culture of human neuronal-glial (HNG) cells stressed using interleukin1-beta (IL-1 beta), and this up-regulation was quenched using specific NF-kB inhibitors including curcumin.