https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 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: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:23032 Sat 24 Mar 2018 07:13:48 AEDT ]]> 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 ]]>