Publications by authors named "M R Namavar"

Article Synopsis
  • Stroke is a major global health issue, mainly causing neuron death through NMDA receptor overactivation, and this study explores IC87201 as a potential treatment to reduce brain damage from ischemic strokes.
  • In an experiment with 24 male rats subjected to cerebral ischemia, researchers compared the effects of IC87201 and Dextromethorphan hydrobromide (DXM) on post-stroke brain recovery.
  • Results indicate that IC87201 significantly improved neurobehavioral functions and reduced brain damage more effectively than DXM, particularly enhancing cell survival in the striatum area of the brain.
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Global cerebral ischemia (GCI) results in damage to the neurons and leads to cognitive impairments. Berberine (BBR) is known for its neuroprotective qualities. This study aimed to investigate the effects of BBR on memory, Blood-brain barrier (BBB) permeability, biochemical factors, and neuronal structure.

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N-methyl-D-aspartate receptor-dependent excitotoxicity is one of the most important mechanisms underlying stroke injury and the resulting neuronal death. In the present study, in order to reduce post-stroke brain injury and improve behavioral performance, a new molecule named IC87201, which acts as an inhibitor of PSD95/nNOS interaction in the intracellular signaling pathway of NMDA receptors, was administered. Using the middle cerebral artery occlusion (MCAO) technique, 24 adult male rats were subjected to one hour of cerebral ischemia.

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Nicorandil is a dual mechanism anti-anginal agent that acts as a nitric oxide (NO) donor and a potassium (K) channel opener. Recent studies have evaluated the effect of nicorandil on ischemic stroke. Neurons have a low tolerance to hypoxia and therefore the brain tissue is significantly vulnerable to ischemia.

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Impaired insulin and growth factor functions are thought to drive many alterations in neurodegenerative diseases like dementia and seem to contribute to oxidative stress and inflammatory responses. Recent studies revealed that nasal growth factor therapy could induce neuronal and oligodendroglia protection in rodent brain damage induction models. Impairment of several growth factors signaling was reported in neurodegenerative diseases.

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