Inhibitory astrocytes-modulating agent that exerts glioprotective effects in cultures and in vivo by decreasing intracellular and extracellular S100B levels.
ONO-2506 (arundic acid; (R)-2-propyloctanoic acid) is an inhibitory astrocytes-modulating agent that exerts glioprotective effects against amyloid-β-peptide (Aβ)-induced glial death in astrocyte cultures (50 μM ONO-2506 against 200 μM Aβ25-35, 24 hr; 1321N1 astrocytes) by decreasing both the intracellular and extracellular S100B levels. Blockade of astrocytic activation by ONO-2506 in vivo is shown to offer therapeutic efficacy in animal models of normal tension glaucoma (10 mg/kg po. mice), spinal cord injury (20 mg/kg/d ip or iv rats), brain seizure, ischemic stroke (10 mg/kg/d ip or iv rats), and Parkinson′s disease (30 mg/kg ip mice).
Mild hypoxia increases ventilation, but severe hypoxia depresses it. The mechanism of hypoxic ventilatory depression, in particular, the functional role of the cerebrum, is not fully understood. Recent progress in glial physiology has provided evidence that astrocytes play active roles
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 22(6), 723-734 (2002-06-05)
A novel agent, (R)-(-)-2-propyloctanoic acid (ONO-2506), has a unique property in that it modulates functions of activated cultured astrocytes, including pronounced inhibition of S-100beta synthesis. The present study examined whether administration of this agent would mitigate the delayed expansion of
Journal of the neurological sciences, 337(1-2), 186-192 (2013-12-24)
Arundic acid (ONO-2506) inhibits the production and release of S100 protein from astrocytes. While numerous studies have assessed the effect of ONO-2506 in the diseased brain, to the best of our knowledge, no study has examined the effect of ONO-2506
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 76, 41-51 (2019-06-17)
Perinatal hypoxia-ischemia (HI) is one of the main causes of mortality and chronic neurological morbidity in infants and children. Astrocytes play a key role in HI progression, becoming reactive in response to the injury, releasing S100 calcium binding protein B
Glutamate is the major excitatory neurotransmitter in the brain, but excessive synaptic glutamate must be removed to prevent excitotoxic injury and death. Two astrocytic glutamate transporters, excitatory amino acid transporter (EAAT) 1 and 2, play a major role in eliminating
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