https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:45031 Wed 26 Oct 2022 10:52:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38877 Wed 23 Feb 2022 10:20:33 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:38875 Wed 23 Feb 2022 09:59:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:44648 2NPs) is on the increase, and so the number of studies dedicated to describing this material's biological effects. Previous studies have presented results indicating the controversial impact of TiO₂NPs on cell fate regarding death and survival. We speculate that this may be due to focusing on each of the subject cells as an isolated individual. In this study, we made a difference by looking at the subject cells as an interrelated population. Specifically, we exposed mesenchymal stem cells (MSCs) to TiO₂NPs and observed cell death and stimulation of proliferation among the cell population. Our data shows that the exposure to TiO₂NPs initiated autophagy, which led to an increase in extracellular Wnt protein levels and increased Wnt/GSK3β/β-catenin/cyclin D1 signalling in the cell population. Autophagy inhibitor repressed the effects of TiO₂NPs, which indicates that ß-catenin regulation was dependent on TiO₂NPs-induced autophagy. The inhibition of β-catenin resulted in dysregulation of cyclin D1 protein expression level. In conclusion, following exposure to TiO₂NPs, MSCs undergo autophagy, which induces cell proliferation among the cell population by upregulation of cyclin D1 through the Wnt/GSK3β/β-catenin pathway.]]> Wed 19 Oct 2022 09:00:38 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34106 Wed 10 Nov 2021 15:13:04 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:36237 Tue 17 Mar 2020 12:25:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36238 Tue 17 Mar 2020 12:25:30 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:30397 Tue 01 May 2018 09:18:50 AEST ]]> 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:32250 Thu 13 Jan 2022 10:31:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25304 Sat 24 Mar 2018 07:30:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25302 Sat 24 Mar 2018 07:30:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:25303 Sat 24 Mar 2018 07:30:19 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:26721 Sat 24 Mar 2018 07:26:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30171 in vitro effects on the human lung cells BEAS-2B following exposure to and oil-dispersant mixtures on human airway BEAS-2B epithelial cells. Here we present the cytotoxic and genotoxic in vitro effects on the human lung cells BEAS-2B following exposure to Corexit dispersants EC9500 and EC9527, Water Accommodated Fraction (WAF) -crude, WAF-9500 + Oil, and WAF-9527 + Oil. Cellular cytotoxicity to WAF-dispersed oil samples was observed at concentrations greater than 1000 ppm with over 70% of observed cellular death. At low concentration exposures (100 and 300 ppm) DNA damage was evidenced by the detection of single strand breaks (SSBs) and double strand breaks (DSBs) as measured by alkaline and neutral comet assay analyses. Immunoblot analyses of the phosphorylated histone H2A.X (ɣ-H2A.X) and tumor suppressor p53 protein confirmed activation of the DNA damage response due to the exposure-induced DNA breaks. Although, many xenobiotics interfere with DNA repair pathways, in vitro evaluation of the nucleotide excision repair (NER) and DSB repair pathways appear to be unaffected by the oil-dispersant mixtures tested. Overall, this study supports that oil-dispersant mixtures induce genotoxic effects in culture.]]> Sat 24 Mar 2018 07:26:16 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:23032 Sat 24 Mar 2018 07:13:48 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24573 50,000 workers. The potential health hazards to these workers may be significant as previous research suggested an association of persistent respiratory symptoms with exposure to oil and oil dispersants. To reveal the potential effects of oil and oil dispersants on the respiratory system at the molecular level, we evaluated the transcriptomic profile of human airway epithelial cells grown under treatment of crude oil, the dispersants Corexit 9500 and Corexit 9527, and oil-dispersant mixtures. We identified a very strong effect of Corexit 9500 treatment, with 84 genes (response genes) differentially expressed in treatment vs. control samples. We discovered an interactive effect of oil-dispersant mixtures; while no response gene was found for Corexit 9527 treatment alone, cells treated with Corexit 9527 + oil mixture showed an increased number of response genes (46 response genes), suggesting a synergic effect of 9527 with oil on airway epithelial cells. Through GO (gene ontology) functional term and pathway-based analysis, we identified upregulation of gene sets involved in angiogenesis and immune responses and downregulation of gene sets involved in cell junctions and steroid synthesis as the prevailing transcriptomic signatures in the cells treated with Corexit 9500, oil, or Corexit 9500 + oil mixture. Interestingly, these key molecular signatures coincide with important pathological features observed in common lung diseases, such as asthma, cystic fibrosis and chronic obstructive pulmonary disease. Our study provides mechanistic insights into the detrimental effects of oil and oil dispersants to the respiratory system and suggests significant health impacts of the recent BP oil spill to those people involved in the cleaning operation.]]> Sat 24 Mar 2018 07:11:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46652 p-NMDAR1) and (3) phosphorylated calmodulin-dependent protein kinase II (p-CaMKII). In addition, the content of whole brain malondialdehyde (MDA) as well as activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined. Treatment with T significantly elevated the number of intact pyramidal cells in hippocampal CA1 region and markedly increased hippocampal protein and mRNA expression levels of p-NMDAR1 and p-CaMK II. Further, T significantly decreased whole brain MDA levels accompanied by elevated activities of SOD and GSH-Px. Data suggest that the protective effects of T on synaptic plasticity in a mouse AD model may be associated with reduction of oxidant stress.]]> Mon 28 Nov 2022 17:29:45 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46651 Ginkgo biloba leaf extract (GbE) is composed predominantly of active ingredients such as flavonoids and terpene lactones and often used to treat cerebrovascular diseases. However, the mechanisms underlying the use of this herbal extract to treat cerebrovascular-mediated damage are not known. The aim of this study was to examine the effectiveness of administration GbE to ameliorate the observed consequences of CIRI. The following parameters were measured: (1) behavioral score (2) infarct area (3) the content of serum malondialdehyde (MDA) as well as activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and (4) interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-a) expression levels in the infarcted brain tissue. Data demonstrated that treatment with GbE to CIRI rats resulted in significant reduction in cerebral-infarcted area associated with improvement in behavioral score. GbE was found to decrease serum MDA levels concomitant with elevated activity levels of SOD and GSH-PX. Immunohistochemistry and Western blot analysis showed that GbE significantly lowered the levels of IL-6 and TNF-a in the infarcted brain tissue. Data suggest that GbE may be therapeutically effective in improving behavioral score in CIRI rats through reduction of oxidative stress and anti-inflammation in the cerebral infarction region.]]> Mon 28 Nov 2022 17:29:30 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46650 Dracocephalum moldevica (DML) was found to exert protective effects on cerebral ischemia-reperfusion injury (CIRI); however, the mechanisms underlying the observed actions of this plant-derived mixture remain to be determined. Thus, the aim of this study was to examine the influence of DML on CIRI rat model induced by middle cerebral artery occlusion (MCAO). The following parameters were measured: (1) viable neurons in the infarcted area using Nissl staining; and (2) immunohistochemistry and Western blot were employed to determine protein expression levels of p53, bcl-2 associated X protein (bax) and B-cell lymphoma-2 (bcl-2), three biomarkers of apoptosis. MCAO significantly decreased the number of viable cortical pyramidal neurons in the infarcted area, while treatment with DML extract significantly elevated the number of viable neurons. MCAO was found to significantly elevate in gene expression levels of p53 and protein expression levels bax accompanied by diminished protein expression levels of bcl-2. Prior administration of DML extract produced marked reduction in gene expression levels of p53 and protein expression levels bax but increased in protein expression levels of bcl-2. Data suggested apoptosis was initiated in MCAO and that DML was effective in treating CIRI via an anti-apoptotic action as evidenced by inhibition of gene expression levels of p53 and protein expression levels of bax with concomitant elevation in protein expression levels of bcl-2. Our findings suggest that extract of DML may prove beneficial in treatment of cerebrovascular disorders.]]> Mon 28 Nov 2022 17:22:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:46649 2NP) following environmental exposure. At present, the consequences of TiO₂NP exposure in bone are not well known. The aim of this study was to investigate the effects of TiO₂NP on mesenchymal stem cells (MSCs) and potential underlying mechanisms. Mesenchymal bone marrow-derived cells were cultured and treated with various concentrations of TiO₂NP. Results showed that TiO₂NP incubation produced cytotoxicity as evidenced by reduced cell viability. Using Western blotting TiO₂NP was found to increase autophagy as determined by elevation in ratio of LC3-II from LC3-I without evidence of necrotic cell death as estimated by lactic dehydrogenase (LDH) level. TiO2NP produced a rise in intracellular reactive oxygen species (ROS) levels. The observed alterations in autophagy and oxidant stress were associated with upregulation of protein expression of p38, JNK, and ERK. Data indicate that TiO₂NP-mediated decrease in MSC survival involves a complex series of events associated stimulation of mitogen-activated protein kinase (MAPK) pathway and consequent autophagy and oxidative damage.]]> Mon 28 Nov 2022 17:22:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32133 in vitro can lead to cell death. At low concentration NaAsO₂ can induce autophagy and at high concentration it can induce apoptosis. The work presented in this poster shows the initial cellular response of human lung epithelial A549 cells to acute exposure to NaAsO₂ in vitro.]]> Mon 23 Sep 2019 12:35:47 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42364 Mon 22 Aug 2022 14:08:37 AEST ]]> 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:34032 Dracocephalum moldavica L. (DML), a Chinese herbal medicine is known to exert protective effects on myocardial ischemia reperfusion injury in rats by inhibiting oxidation damage and inflammatory reactions. However, the effectiveness of DML in cerebral ischemia reperfusion injury (CIRI) as a protective substance and the underlying mechanisms remain to be determined. The aim of this study was thus to examine the influence of DML on CIRI using a rat model induced by 2-h transient middle cerebral artery occlusion (MCAO) produced by intraluminal suture blockade followed by 22 h reperfusion. The parameters determined include neurological behavior, histochemical assessment of cerebral infarct volume, and determination of various metabolic biomarkers. Data showed that DML markedly improved neurobehavioral scores and reduced cerebral edema and infarction. In addition, DML significantly reduced malondialdehyde (MDA) content and elevated activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), in addition, marked decrease in levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-a (TNF-a). Data suggest that the protective effects of DML on CIRI may be related to processes involving antioxidation and anti-inflammation.]]> Mon 04 Feb 2019 11:46:05 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34031 Herba cistanche, are known to exert protective effects on cognitive deficits in Alzheimer's disease (AD); however, the underlying mechanisms of this herbal extract on cognitive performance remain unclear. The aim of this study was thus to examine the protective mechanism attributed to PhG on cognitive deficits in an AD senescence accelerated mouse prone 8 (SAMP8) model. Cognitive deficit parameters examined included (1) Morris water maze (MWM) assessing cognitive performance and (2) quantification of dendritic spine density in hippocampal CA1 region by Golgi staining, a molecular biomarker of synaptic function. In addition, levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and gluthathione peroxidase (GSH-Px) were determined to examine the potential role of oxidant processes in cognitive dysfunction. Data showed that PhG significantly decreased escape latency and path length, associated with a rise in the percentage of time spent in the target quadrant and number of platform crossings. In addition, PhG significantly increased dendritic spine density in the hippocampal CA1 region accompanied by elevated expression levels of synaptophysin (SYN) and post synaptic density 95 (PSD-95), reduced MDA content, and elevated the activities of SOD and GSH-Px. Data suggest that the ability of PhG to ameliorate cognitive deficits in SAMP8 mice may be related to promotion in synaptic plasticity involving antioxidant processes.]]> Mon 04 Feb 2019 11:38:53 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33955 Amygdalus mongolica contain various constituents including flavonoids and vitamin E, which are known to exert antioxidant effects. However, the safety of the oil extract of this compound is not fully known. The aim of this study was to determine the physicochemical properties of A. mongolica oil, identify the constituents and subsequently assess the effectiveness of utilizing this seed extract in hyperlipidemia as an antioxidant agent. In particular, the toxicity and safety of A. mongolica oil were examined with emphasis on effects on blood lipids level and serum lipid peroxidation using a hyperlipidemia rat model. Treatment with 20 ml/kg A. mongolica oil produced no apparent adverse effects after 14 days in normal female and male rats. A dose of 2.5-10 ml/kg A. mongolica oil administered to hyperlipidemic male rats significantly decreased serum total cholesterol (TC), low-density lipoprotein-C (LDL-C), malondialdehyde (MDA), total cholesterol high-density lipoprotein-C (TC/HDL-C), LDL-C/HDL-C, and atherosclerosis index(AI). In contrast, glutathione (GSH) levels and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly increased. Data demonstrated that A. mongolica oil may be utilized in conditions of hyperlipidemia due to its antioxidant effects.]]> Fri 25 Jan 2019 11:54:00 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:42217 Fri 19 Aug 2022 11:21:32 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32496 Fri 08 Jun 2018 16:14:20 AEST ]]>