https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30125 Wed 11 Apr 2018 14:40:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30603 Wed 09 Mar 2022 15:58:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32468 1-42). In particular, the purpose of this investigation was to examine alterations in mRNA and protein expression of DNMT. Data demonstrated that schisandrin B blocked Aß_1-42-mediated injury in SH-SY5Y neuronal cell line as evidenced by a restoration of cellular morphology and cell viability to approximate control levels at the highest 10 µg/ml Schisandrin B. Incubation with Aß_1-42 significantly decreased mRNA and protein expression of DNMT3A and DNMT1 in SH-SY5Y neuronal cell line. Incubation with Aß_1-42 followed by 24 treatment with schisandrin B significantly inhibited the Aß_1-42 -induced changes in mRNA and protein expression of DNMT3A and DNMT3B in a concentration-dependent manner. It is of interest that the mRNA expression of DNMT3A and DNMT1 were significantly higher than control. Data thus indicate schisandrin B was effective in inhibiting the actions of Aß_1-42 on cell survival and morphology and that DNA methylation may be associated with the beneficial findings.]]> Wed 06 Jun 2018 14:05:00 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:43940 Wed 05 Oct 2022 12:51:29 AEDT ]]> 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 Aβ_1-42 significantly reduced cell viability. Treatment with Schisandrin to Aβ_1-42 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 Aβ_1-42 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 Aβ_1-42 -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 ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35913 Thu 16 Jan 2020 14:28:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26413 1-40 (5 μmol/L) protein is considered to be a model of AD. Hence the aim of this study was to examine the influence of Schizandrol A, a plant extract, on DNA methylation in SH-SY5Y cells exposed to Aβ_1-40. Aβ_1-40 were incubated with varying concentrations of Sehizandrol A to a final concentration of 1 (low), 3 (intermediate) or 9 μg/ml (high). Exposure of SH-SY5Y with Aβ1-40 reduced viability, and altered cellular morphology and mRNA expression of DNA methyltransferase (DNMT3A) and DNMT3B. Treatment with 1 or 3 μg/ml Sehizandrol A resulted in normal cell morphology as well as elevated cell number, enhanced viability, and increased mRNA expression of DNMT3A and DNMT3B compared to saline. However, an increase in Sehizandrol A to 9 μg/ml produced a fall in cell viability, as well as a decrease in mRNA DNMT3A and DNMT3B expression to control levels. Data demonstrated that Schizandrol A at 1 or 3 μg/ml improved cell morphological appearance and viability of Aβ_1-40 injured SH-SY5Y cells by an enhanced DNA methylation pathway.]]> Sat 24 Mar 2018 07:27:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26320 Sat 24 Mar 2018 07:24:13 AEDT ]]> 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 ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32496 Fri 08 Jun 2018 16:14:20 AEST ]]>