Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Repeated ischemic insults at one hour intervals result in more severe neuronal damage than a single similar duration insult. The mechanism for the more severe damage with repetitive ischemia is not fully understood. We hypothesized that the prolonged reperfusion periods between the relatively short ischemic insults may result in a pronounced generation of oxygen free radicals (OFRs). In this study, we tested the protective effects of superoxide dismutase (SOD) and catalase (alone or in combination), and U78517F in a gerbil model of repetitive ischemia. Three episodes (two min each) of bilateral carotid occlusion were used at one hour intervals to produce repetitive ischemia. Superoxide dismutase and catalase were infused via osmotic pumps into the lateral ventricles. Two doses of U78517F were given three times per animal, one half hour prior to each occlusion. Neuronal damage was assessed 7 days later in several brain regions using the silver staining technique. The Mann-Whitney U test was used for statistical comparison. Superoxide dismutase showed significant protection in the hippocampus (CA4), striatum, thalamus and the medial geniculate nucleus (MGN). Catalase showed significant protection in the striatum, hippocampus, thalamus, and MGN and the substantia nigra reticulata. Combination of the two resulted in additional protection in the cerebral cortex. Compared to the controls, there was little protection in a dose of 3 mg/kg of U78517F. There was significant protection with a dose of 10 mg/kg in the hippocampus (CA4), striatum, thalamus, medial geniculate nucleus and the substantia nigra reticulata.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Superoxide dismutase, catalase, and U78517F attenuate neuronal damage in gerbils with repeated brief ischemic insults. 806 23

Curcuma comosa Roxb. is widely used as a gynaecological traditional medicine in South-East Asia and recent behavioral studies have shown that C. comosa extract significantly improved the spatial memory in rats. The present study investigated the protective effects of Curcuma comosa hexane extract on the ethanol (EtOH)-induced oxidation in rat brains. Young female Wistar rats were given 20% of EtOH intraperitoneally to induce the oxidative stress. Subsequently, C. comosa hexane extract was intraperitoneally co-administered at the doses of 100 and 250 mg kg(-1) b.wt. to the EtOH-induced rats for 14 days. The neuron densities of CA1, CA3 and CA4 areas of the hippocampus were counted and the activities of hippocampal Catalase (CAT), Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) were determined. EtOH significantly decreased the neuron densities in Cornu Ammonis (CA), including CA1 and CA3 areas; however, the decrease was prevented by C. comosa co-administration. EtOH administration also increased the CAT and GPx activities in the hippocampus which were reversed by C. comosa co-administration. Moreover, C. comosa administration increased the SOD activity in a dose-dependent manner in the EtOH treated groups. C. comosa prevented the neuron loss in the hippocampus caused by EtOH. The possible neural protective mechanism may involve with the changes in activities of the antioxidant enzymes in the hippocampus.
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PMID:Curcuma comosa prevents the neuron loss and affects the antioxidative enzymes in hippocampus of ethanol-treated rats. 2419 65