https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 The protective underlying mechanisms of Schisandrin on SH-SY5Y cell model of Alzheimer's disease https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44238 1-42) peptide 10 μmol/L was used to induce in vitro AD model in SH-SY5Y. Exposure to Aβ1-42 significantly reduced cell viability. Treatment with Schisandrin to Aβ1-42 exposed cells increased cell viability compared to amyloid peptide; however only the 10 μmol/L Schisandrin concentration was effective in restoring cell viability to control. Western blot analysis demonstrated that Aβ1-42 produced a significant decrease in p-Akt protein expression levels accompanied by marked elevation in p-tau and p-GSK-3β protein expression levels. Addition of 10 μmol/L Schisandrin to amyloid-treated SH-SY5Y cells was found to significantly increase protein expression levels of p-Akt associated with reduction in expression levels of p-tau and p-GSK-3β protein. Treatment with 10 μmol/L Schisandrin of SH-SY5Y cells with the p-Akt inhibitor LY294002 demonstrated that the herbal-induced rise in p-Akt protein expression was diminished by this inhibitor indicating that signal transduction occurred in the observed cellular effects. Evidence indicates that Schisandrin inhibition of Aβ1-42 -mediated cellular damage in AD neurons may involve activation of the PI3K/Akt signaling pathway where up-regulation of p-Akt activity consequently leads downstream to decreased activity of p-GSK-3β phosphorylation accompanied by reduced tau protein. Consequently, restoration of neuronal cell viability was noted. Our findings suggest that the use of Schisandrin may be considered beneficial as a therapeutic agent in AD.]]> Tue 11 Oct 2022 11:46:31 AEDT ]]> Differentially expressed long-chain noncoding RNAs in human neuroblastoma cell line (SH-SY5Y): Alzheimer's disease cell model https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36871 1 or log2 (multiple change) < −1 had statistical significance (P< .05). The differential expression profiles of amyloid (Aβ)-treated SH-SY5Y cells showed 40 lncRNA were up-regulated, while 60 lncRNA were down-regulated. GO and KEGG analysis demonstrated that differentially expressed genes were predominantly involved in the mitogen-activated protein kinase (MAPK) signaling pathway, p53 signaling pathway, hepatitis B, cell cycle, post-translational protein modification, and regulation. In conclusion, approximately 100 dysregulated lncRNA transcripts were found in amyloid (Aβ)-treated SH-SY5Y cells and these lncRNAs may play an important role in the occurrence and development of AD through altered signal pathways.]]> Mon 13 Jul 2020 16:25:43 AEST ]]>