Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral ischemia leads to memory impairment, and several studies have indicated that physical exercise (PE) has memory-improving effects after ischemia. This study was designed to further explore the specific role of PE in novel object recognition (NOR) memory after stroke and the exact cortical regions in which memory is restored by PE. Spontaneously hypertensive rats (SHR) were subjected to transient middle cerebral artery occlusion (tMCAO) or sham surgery, followed by 26 days of PE starting on day 3 post-tMCAO. Thereafter, infarct volume, neurobehavioral outcome and NOR memory were assessed. Immunofluorescence staining and Luxol Fast Blue (LFB) staining were performed in the prefrontal cortex, entorhinal cortex and corpus callosum regions. Western blot analysis was performed to detect expressions of Nestin, Bcl-2 and SYN proteins in the entorhinal cortex. After tMCAO, NOR memory impairment was found in SHR. Rats subjected to PE post-tMCAO showed increased discrimination ratio, as well as significant decreases in infarct volumes and modified neurological severity scores (mNSS), when compared with tMCAO rats without PE. After stroke, NeuN-positive cell number was drastically reduced in the entorhinal cortex, rather than in the prefrontal cortex. Ischemic stroke had no impact on myelin and phospholipids, and the ratio of SMI-32/MBP in the corpus callosum. PE increased NeuN, Nestin, Ki67, MBP, SYN, PSD-95 and Bcl-2 expressions in the entorhinal cortex, while TUNEL and SMI-32 expressions were decreased. In conclusion, the NOR memory-improving capacity promoted by PE was closely related to neuronal cell proliferation and synaptic plasticity of the entorhinal cortex.
 ...
PMID:Physical Exercise Promotes Novel Object Recognition Memory in Spontaneously Hypertensive Rats after Ischemic Stroke by Promoting Neural Plasticity in the Entorhinal Cortex. 2916 35

Bone marrow mesenchymal stem cells (BMSCs) are mainly administered via three routes: intra-arterial, intravenous and intracerebral. It has been reported that BMSC administration via each route ameliorates the functional deficits after cerebral ischemia. However, there have been no comparisons of the therapeutic benefits of BMSC administration through different delivery routes. In this study, we injected BMSCs into a rat model of transient middle cerebral artery occlusion (MCAO) through the intra-arterial, intravenous, or intracerebral route at day 7 after MCAO. Control animals received only the vehicle. Neurological function was assessed at post-ischemic days (PIDs) 1, 7, 14, 21, 28 and 35 using behavioral tests (modified Neurological Severity Score (mNSS) and the adhesive removal test). At PID 35, the rat brain tissues were processed for histochemical and immunohistochemical staining. Our results showed that BMSC transplantation via the intra-arterial, intravenous, and intracerebral routes induced greater improvement in neurological functions than the control treatments; furthermore, the intra-arterial route showed the greatest degree and speed of neurological functional recovery. Moreover, BMSCs treatment through each route enhanced reconstruction of axonal myelination in the area of the corpus callosum on the infarct side of the cerebral hemisphere, increased the expression of SYN and Ki-67, and decreased the expression of Nogo-A in the brain. These effects were more apparent in the intra-arterial group than in the intravenous and intracerebral groups. These data suggest that BMSCs transplantation, especially through intra-arterial delivery, can effectively improve neurological function intra-arterial. The underlying mechanism may include the promotion of synaptogenesis, endogenous cell proliferation, and axonal regeneration.
 ...
PMID:Comparisons of the therapeutic effects of three different routes of bone marrow mesenchymal stem cell transplantation in cerebral ischemic rats. 2927 77

Ischemic stroke is the second leading cause of death worldwide. Ischemia-induced cognitive dysfunction may result in a poor quality of life. Synaptic plasticity plays a key role in cognition promotion. An enriched environment (EE), which can attenuate cognitive deficits in chronic cerebral hypoperfusion, has been shown to facilitate synaptic plasticity. However, the effect of EE on synaptic plasticity in bilateral cerebral hemispheres in stroke remains unclear. This study used a permanent middle cerebral artery occlusion mouse model, which was divided into standard housing and EE groups. The Morris water maze test was performed to detect the cognitive function. Electron microscopy was used to determine the synapse numbers. The expression of SYN and GAP-43 was then quantified by immunofluorescence staining and Western blot analysis. Compared with the standard housing, EE promoted the cognitive function recovery in the mice with stroke. Moreover, EE increased the synapse numbers and the expression of SYN and GAP-43 in both the ipsilateral and contralateral hemispheres (P < 0.05). A further correlation analysis revealed a positive correlation between the cognitive function outcomes and the relative expression of GAP-43 and SYN. Furthermore, the correlation of the expression of GAP-43 and SYN with cognitive function was higher in the contralateral brain than in the ipsilateral brain. In conclusion, an EE may promote cognitive function via bilateral synaptic remodeling after cerebral ischemia. Also, the contralateral brain may play an important role in the recovery of cognitive function.
 ...
PMID:Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia. 3178 Oct 25