ha-1100 has been researched along with Ischemic-Attack--Transient* in 1 studies
1 other study(ies) available for ha-1100 and Ischemic-Attack--Transient
| Article | Year |
|---|---|
Rho-kinase inhibitor prevents acute injury against transient focal cerebral ischemia by enhancing the expression and function of GABA receptors in rats.
Studies have shown hydroxyfasudil-mediated inhibition of Rho-kinase (ROCK) has efficacy in rodent models of focal ischemia and in in vitro systems that recapitulate stroke conditions. However, the mechanisms underlying the neuroprotective effects of the ROCK inhibitor on stroke are not well understood. In this study, we examined the role of γ-aminobutyric acid (GABA) interneurons in the effects of hydroxyfasudil on transient middle cerebral artery occlusion (tMCAO) induced acute ischemia-reperfusion injury to explore the mechanisms. tMCAO rats developed marked neurological deficits and impaired long-term potentiation; these effects were attenuated by hydroxyfasudil. Expression of GABA Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; CA1 Region, Hippocampal; Gene Expression Regulation; Ischemic Attack, Transient; Long-Term Potentiation; Male; Neuroprotective Agents; NF-kappa B; Phosphorylation; Protein Kinase Inhibitors; PTEN Phosphohydrolase; Rats; Rats, Sprague-Dawley; Receptors, GABA-A; Receptors, GABA-B; rho-Associated Kinases; Synapses; Time Factors | 2017 |