Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, we have identified the alteration in the expressions of GABA shunt-associated enzymes and the GABA transporter in order to determine the relationship between the neuronal damage and GABA metabolism following ischemia. At 30 min post-ischemia, the immunoreactivities of the glutamic acid decarboxylase (GAD) isoforms were markedly elevated in the CA1 region, as compared with the sham operated group. At 3-12 h post-ischemia, their immunoreactivities recovered at the sham level. These patterns were similarly observed up to 12 h following ischemia insult. However, the intensity of GAD67 was markedly increased at 24 h post-ischemic insult. The temporal changes in GABA transporter 1 (GAT-1) expressions were similar to that of GAD67, but not GAD65, expression, at least prior to 12 h after ischemic insults. GAT-1 immunoreactivity was significantly elevated in the CA1 region posterior to 12 h post-ischemia. Both succinic semialdehyde dehydrogenase (SSADH) and succinic semialdehyde reductase (SSAR) immunoreactivities were not altered in GABAergic neurons following ischemia. In contrast, in pyramidal cells, both SSADH and SSAR immunoreactivities showed chronological alterations in the CA1 region. Thus, our findings suggest that the differential alterations of GABA metabolism may be one of the important factors in neuronal damages induced by ischemia.
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PMID:Spatial and temporal alterations in the GABA shunt in the gerbil hippocampus following transient ischemia. 1210 61

Seleno-organic compound, ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), is a substrate with radical-scavenging activity. In this study, we observed the neuroprotective effects of ebselen against ischemic damage and on GABA shunt enzymes such as glutamic acid decarboxylase 67 (GAD67), GABA transaminse (GABA-T) and succinic semialdehyde dehydrogenase (SSADH) in the hippocampal CA1 region after 5 min of transient forebrain ischemia in gerbils. For this, vehicle (physiological saline) or ebselen was administered 30 min before or after ischemia/reperfusion and sacrificed 4 days after ischemia/reperfusion. The administration of ebselen significantly reduced the neuronal death in the CA1 region induced by ischemia/reperfusion. In addition, treatment with ebselen markedly elevated GAD67, GABA-T and SSADH immunoreactivity and their protein levels compared to that in the vehicle-treated group, respectively. These results suggest that ebselen protects neurons from ischemic damage via control of the expressions of GABA shunt enzymes to enter the TCA cycle.
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PMID:Neuroprotection of ebselen against ischemia/reperfusion injury involves GABA shunt enzymes. 1957 96