ro-25-6981 and Reperfusion-Injury

ro-25-6981 has been researched along with Reperfusion-Injury* in 1 studies

Other Studies

1 other study(ies) available for ro-25-6981 and Reperfusion-Injury

ArticleYear
Neuroprotection of Ro25-6981 Against Ischemia/Reperfusion-Induced Brain Injury via Inhibition of Autophagy.
    Cellular and molecular neurobiology, 2017, Volume: 37, Issue:4

    In this study, we investigated the neuroprotective effect of Ro25-6981 against cerebral ischemia/reperfusion injury. Ro25-6981 alone or in combination with rapamycin was intracerebroventricularly administered to rats which suffered transient forebrain ischemia inducing by 4-vessel occlusion and reperfusion. Nissl staining was used to determine the survival of CA1 pyramidal cells of the hippocampus, while immunohistochemistry was performed to measure neuron-specific enolase (NSE) expression. The expression of autophagy-related proteins, such as microtubule-associated protein l light chain 3 (LC3), Beclin 1, and sequestosome 1 (p62), was assessed by immunoblotting. Nissl staining showed that neuronal damage was reduced in the hippocampal CA1 pyramidal layer in rats that received Ro25-6981. The protective effect of Ro25-6981 was dose-dependent, with a significant effect in the middle-dose range. The expression of NSE increased after Ro25-6981 treatment. Ro25-6981 significantly decreased LC3II (which is membrane bound) and Beclin 1, and increased p62. In addition, Ro25-6981 decreased rapamycin-induced neuronal damage and excessive activation of autophagy after I/R. Taken together, the results suggest that Ro25-6981 could suppress ischemic brain injury by regulating autophagy-related proteins during ischemia/reperfusion.

    Topics: Animals; Apoptosis Regulatory Proteins; Autophagy; Brain; Brain Injuries; Brain Ischemia; Disease Models, Animal; Male; Microtubule-Associated Proteins; Neuroprotection; Neuroprotective Agents; Phenols; Piperidines; Rats, Sprague-Dawley; Reperfusion Injury

2017