The findings emphasize the need to explore the role of psychological factors, and include gender, in driving studies and models.”
“Hyperglycemia, which occurs under the diabetic PR-171 concentration condition, is widely recognized as the causal link between diabetes and its serious complications. Diabetic neuropathies, which are among the most frequent complications of diabetes, affect sensory, motor, and autonomic nerves. The exact molecular
mechanisms of high glucose-induced toxicity on neuronal cells, is still unclear. We previously reported that high glucose can induce apoptosis in PC12 cells, as evidenced by DNA fragmentation and high Bax/Bcl-2 ratio. The present study examined the involvement of caspase-3, the executioner, and two initiators of apoptosis, caspase-8 and caspase-9, during
high glucose-induced apoptosis in PC12 cells, a neuronal cell line. Cells were exposed to high glucose with or without z-VAD-fmk, a pan-caspase inhibitor. Cell viability was measured by MTT assay. Caspase activity was determined spectrophotometrically using enzyme specific substrates. Selleckchem GW4869 To correlate and confirm the caspase activity with changes in protein expression, procaspase-8, -9, and -3 were evaluated by Western blot analysis. The DNA-fragmentation was determined by DNA ladder using gel electrophoresis. The PC12 cell viability on high glucose exposure was decreased compared to controls, which was reversed by z-VAD-fmk. The activities of caspase-8, -9, and -3 were significantly increased in treated cells compared to controls. Moreover, high glucose exposure induced a significant decrease in protein levels of procaspases, indicating
conversion of pro-form into the mature caspases. Finally, DNA fragmentation (Ladder) was shown in treated cells by high glucose. Based on the current data, it could be concluded that high glucose-induced apoptosis Etomidate in PC12 cells is mediated, in part, by activation of caspase-8, -9, and -3 dependent pathways. (C) 2009 Published by Elsevier Ireland Ltd.”
“The present study investigated the effects of acute aerobic exercise on cognitive brain functions of older adults. Twenty-four males (12 older and 12 younger adults) performed a modified flanker task during a baseline session (no exercise) and after light and moderate cycling exercise in counterbalanced order on different days while measures of task performance and the P3 component of an event-related brain potential were collected. The results indicated that, for both age groups, reaction time following moderate exercise was shorter relative to the other sessions, and P3 latencies following both light and moderate exercise were shorter compared with the baseline session. In contrast, P3 amplitude increased only following moderate exercise in younger adults.