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

The aim of this study was to assess the role of nitric oxide (NO) in lipid peroxidation following 5 min of bilateral carotid occlusion in the Mongolian gerbil. The study consisted of 4 experimental groups (n = 10). Animals were either sham operated, subjected to bilateral carotid occlusion or administered the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg i.p.) 30 min, 6, 24 and 48 h following sham operation or 5 min bilateral carotid occlusion. Animals were killed 96 h post surgery and changes in the concentrations of malonaldehyde and 4 hydroxyalkenals (the main decomposition products of peroxides derived from polyunsaturated fatty acids and related esters) were measured in the hippocampus and cortex using the LPO-586 colorimetric method. The results showed a significant increase in the concentrations of both decomposition products following 5 min of bilateral carotid occlusion. L-NAME administered to sham operated controls had no effect, but in those animals subjected to 5 min of bilateral carotid occlusion L-NAME significantly decreased the levels of both decomposition products. These results suggest that inhibition of NO synthase activity decreases lipid peroxidation in the gerbil model of cerebral ischaemia.
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PMID:NG-nitro-L-arginine methyl ester protects against lipid peroxidation in the gerbil following cerebral ischaemia. 856 40

The neuroprotective effects of spiramine T, an atisine-type diterpenoid alkaloid isolated from the Chinese herbal medicine Spiraea japonica var. acuta (Rosaceaee), on cerebral ischemia-reperfusion injury produced by 10-min bilateral occlusion of the common carotid arteries followed by 5-day reperfusion in gerbils were investigated. Intravenous spiramine T (0.38, 0.75, and 1.5 mg.kg-1) markedly reduced the stroke index, enhanced the recovery of EEG amplitude during reperfusion and decreased the concentrations of cortex calcium and LPO in a dose-dependent manner. However, no significant effects on water and sodium contents were observed. These results suggested that spiramine T exhibited protective effects on cerebral ischemia-reperfusion injury in gerbils, and its mechanism might be related to reducing calcium accumulation and lipid peroxidation. This is the first report on spiramine T as a natural product with neuroprotective effects.
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PMID:Neuroprotective effects in gerbils of spiramine T from Spiraea japonica var. acuta. 1130 60

Chronic cerebral ischemia was induced by ligation of both common carotid arteries in Wistar rats, divided by sensitivity to hypoxia into highly sensitive and low-sensitive. Noopept (peptide preparation), injected (0.5 mg/kg) during 7 days after occlusion of the carotid arteries, reduced the neurological disorders in rats with high and low sensitivity to hypoxia and improved their survival during the postischemic period. Noopept normalized behavior disordered by cerebral ischemia (according to the open field and elevated plus maze tests), prevented accumulation of LPO products and inhibition of antioxidant systems in the brain of rats with high and low sensitivity to hypoxia. Hence, noopept exhibited a neuroprotective effect in cerebral ischemia.
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PMID:Noopept reduces the postischemic functional and metabolic disorders in the brain of rats with different sensitivity to hypoxia. 1952 57

The antioxidant effect of an adenosine A1 receptor agonist cyclopentyladenosine was studied on the model of focal cerebral ischemia. Ischemic injury of the brain was accompanied by changes in LPO processes (in the blood and brain tissue) and failure of some factors for antioxidant protection (peroxidase and catalase) that inactivate reactive metabolites. Changes in the ratio between LPO and antioxidant protection were less pronounced after treatment with cyclopentyladenosine.
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PMID:Effect of cyclopentyladenosine on lipid peroxidation during focal cerebral ischemia. 2495 91

Parkinson disease occurs due to the depletion of dopaminergic neurons in brain resulting in decreased dopamine level and abnormal protein aggregation. Chrysin is a flavonoid which possesses pharmacological properties against various diseases like hypertension, diabetes, cancer, etc. According to the recent literatures, it is evidenced that chrysin protects mice against Focal Cerebral Ischemia/Reperfusion Injury. The present study aimed to elucidate the effect of chrysin on neuronal restoration in MPTP intoxicated acute mice model. From the results, it is revealed that the pre-treatment with chrysin protected MPTP induced degeneration of nigra-striatal neurons. It is observed that chrysin also ameliorates MPTP induced oxidative stress in mice by upregulating GSH, SOD and downregulating LPO levels. The motor dysfunction is also found to be enhanced which was evidenced through Beam walk, Horizontal grid and vertical grid tests. Pre-treatment with chrysin also averted MPTP induced alterations in neurotrophic factors, inflammatory markers and Dopamine contents. The findings of the present study clearly indicated that the chrysin reversed the neurochemical deficits, oxidative stress and behavioral abnormalities in PD mice and offers promising strategy for the treatment of neurodegenerative diseases.
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PMID:Chrysin restores MPTP induced neuroinflammation, oxidative stress and neurotrophic factors in an acute Parkinson's disease mouse model. 3132 81