[Show abstract][Hide abstract] ABSTRACT: We assessed whether chronic treadmill exercise attenuated restraint stress-induced cognition impairment. Although serum corticosterone was not significantly altered by exercise, the restraint-induced increases in hippocampal malondialdehyde (MDA) and 4-hydroxynonenal (HNE) were reduced by chronic exercise. The exercise paradigm also reversed stress-induced reductions in brain-derived neurotrophic factor (BDNF), which increased cAMP response element-binding protein (CREB) and AKT activation. We verified the relationship between oxidative stress and BDNF signaling by treating primary hippocampal cultures with hydrogen peroxide (H2O2), which reduced BDNF and phosphorylated CREB and AKT (p-CREB, p-AKT) in a dose-dependent manner. Notably, pretreatment with N-etylcysteine (NAC) reversed these decreases in a dose-dependent manner. These findings suggest that chronic exercise can ameliorate repeated stress-induced cognitive impairment by detoxifying reactive oxygen species (ROS) in the hippocampus and activating BDNF signaling.
Biochemical and Biophysical Research Communications 03/2013; 434(2). DOI:10.1016/j.bbrc.2013.02.111 · 2.30 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To correlate collateral flow on multiphasic contrast enhancement computed tomography (CT) and graded ischemic changes on diffusion weighted MR in patients with acute middle cerebral artery (MCA) infarction.
A retrospective evaluation of diffusion weighted images (DWIs) and three phasic contrast enhanced CT (CECT) was performed on 11 patients with MCA occlusions. The area of ischemic change on DWIs was graded according to the Alberta Stroke Program Early CT Score (ASPECTS) criteria. To evaluate collateral flow on three phasic CECT, we counted the number of contrast enhancing MCA branches distal to the occlusion site at the sylvian fissure from predetermined axial images. The collateral ratios of counted numbers to those at the normal side were calculated at each phase (CR1, CR2, CR3). We then compared collateral ratios from the three phasic CECT with ASPECTS data from DWIs.
Collateral ratios from the three phasic CECT were determined to be CR1 .48 ± .27, CR2 .73 ± .36 and CR3 .72 ± .30. We discovered a correlation between both the CR2 and ASPECTS (r= .675, P= .023) and the CR3 and ASPECTS (r= .664, P= .026).
The number of contrast enhancing branches distal to the MCA occlusion, as counted in the sylvian fissure on later phase images of multiphasic CECT, reflects the status of collateral flow, and correlates with ASPECTS on DWIs.
Journal of neuroimaging: official journal of the American Society of Neuroimaging 07/2011; 21(3):225-8. DOI:10.1111/j.1552-6569.2010.00496.x · 1.73 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background : Chronic cerebral hypoperfusion induced by permanent occlusion of bilateral common carotid arteries (2VO) in rats caused cognitive deficits and neuronal damage. Cyclooxygenase-2 (COX-2) inhibitor was reported to attenuate both post-ischemic prostaglandin accumulation and neuronal damage. We studied the expression of mRNA of COX-2 in the hippocampus during hypoperfusion and the effectiveness of selective cyclooxygenase-2 inhibitor, rofe - coxib, in preventing the neuronal damage of this model. Methods : Bilateral common carotid arteries of the rat were ligated with silk sutures. The expression of mRNA for COX-1 and COX-2 were detected by the RT-PCR. The first group of animals (n=6) was treated with rofecoxib (10 mg/kg, i.p.) 7 days after operation and the following 7 days. The second group of animals (n=6) was treated with diclofenac sodium (9mg/kg, i.p.) and the third group of animals (n=5) was treated with vehicle (DMSO). TdT-mediated dUTP nick end labeling (TUNEL) technique was performed to esti- mate delayed cell death. Results : Bilateral carotid artery occlusion (2VO) was shown to induce apoptotic morphology and DNA strand break in hippocampal neurons from 7 days with a peak at 14, 28 days. mRNA of COX-2 appeared in the frontal cortex (14, 28 days) and hippocampus (14, 28, 63 days). Treatment with rofecoxib significantly (p