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Target Concepts:
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Query: UMLS:C0917798 (
cerebral ischemia
)
17,036
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cerebral ischemia
is known to induce endogenous adaptive mechanisms such as the activation of ATP-sensitive potassium channels that can prevent or delay neuronal injury. This process can be therapeutically mimicked by treatment with potassium channel openers. Primary neuronal cell cultures were derived from embryonic chick telencephalon and were exposed to chemical hypoxia (1 mM cyanide) or excitotoxic injury (1 mM L-glutamate). While treatments with the potassium channel openers bimakalim (1-10 microM) and
EMD
57283 (0.1-10 microM) were clearly able to maintain neuronal viability after chemical hypoxia, similar concentrations of the drugs had negligible effects on glutamate-induced neurotoxicity. In contrast, both types of neuronal injury were sensitive to the protective action of the glutamate receptor antagonist dizocilpine (MK-801; 0.1-1 microM). The neuroprotective effect of bimakalim against chemically induced hypoxic injury was reversed by tolbutamide (1 microM), an ATP-sensitive potassium channel blocker. These experiments demonstrate neuroprotective effects of potassium channel openers that could be related to inhibition of neurotransmitter release.
...
PMID:Activation of ATP-sensitive potassium channels decreases neuronal injury caused by chemical hypoxia. 909 18
Diabetes causes various macrovascular and microvascular alterations, often culminating in major clinical complications (first of all, stroke) that lack an effective therapeutic intervention.
N
-palmitoylethanolamide-oxazoline (PEA-OXA) possesses anti-inflammatory and potent neuroprotective effects. Although recent studies have explained the neuroprotective properties of
PEA
-OXA, nothing is known about its effects in treating
cerebral ischemia
.
...
PMID:
N
-Palmitoylethanolamide-Oxazoline Protects against Middle Cerebral Artery Occlusion Injury in Diabetic Rats by Regulating the SIRT1 Pathway. 3156 58