The molecular and ultrastructural aspects of the formation of mitochondrial dysfunction in the modeling of chronic cerebral ischemia: The mitoprotective effects of Angiolin

Abstract

Modeling of cerebral circulation disorder by bilateral occlusion of carotids was accompanied by formation of severe neurological symptoms and their preservation for up to 18 days of the experiment. We found a significant decrease in the level of the HSP₇₀ heat shock protein and the formation of persistent mitochondrial dysfunction. Administration of Angiolin to experimental animals resulted in activation of the expression of the HSP₇₀ gene in neurons and ultrastructural improvement of mitochondria and neurons of CA1 hippocampal zone. The substantial mitoprotective activity of Angiolin is based on its antioxidant activity and the ability to positively influence the activity of anaerobic glycolysis, thus stabilizing the cellular energy metabolism under conditions of ischemic injury.