Changes at the focus of experimental ischemic stroke treated with neuroprotective agents

Abstract

The aim of the present work was to compare the morphological changes occurring at the focus of experimental ischemic stroke treated with agents of the neurotrophic group (alpha-GPC, cerebrolysin), an agent with nootropic properties (piracetam), and a mixed-action agent (vinpocetine). Experiments were performed on 18 rats. Transient cerebral circulatory lesions (acute ischemia) were produced in the right hemisphere by clipping the stem of the innominate artery for 40 min. Light microscopic and electron microscopic studies were performed on fragments of cerebral cortex, brainstem, and cerebellum. Use of alpha-GPC and cerebrolysin increased the tolerance of neurons to ischemic damage and slowed the execution of the cell death program. Intracellular changes were seen and were interpreted as adaptive and reparative: these included folding of the nuclear membrane, abundance of polyribosomes, and endoplasmic reticulum and Golgi complex hypertrophy. These agents preserved the structures of the nuclear membranes and major cellular organelles. When piracetam and vinpocetine were used, all morphological measures indicated inadequate energy provision for repair processes in the acute stage of ischemic stroke. Morphological signs of functional tension of cerebral cortex neurons were seen, with gliocytes in different stages of apoptosis, along with the phenomenon of incomplete separation of gliocytes during proliferation, pathological changes to myelin and non-myelinated fibers, and abnormalities in synapse structure.

Peripheral inflammatory activation after hippocampus irradiation in the rat

“…Here, we took into consideration the previous fi nding that pretreatment with phosphatidylcholine (PC) prevented the decrease in hippocampal neurogenesis after a lipopolysaccharide-induced peripheral infl ammatory challenge (T ő k é s et al 2011). L-alpha-glycerylphosphorylcholine (GPC) is a water-soluble, deacylated PC derivative, which has proved eff ective against the loss of the membrane function in CNS injuries (Amenta et al 1994, Onishchenko et al 2008. Against this background, experiments were undertaken to characterize the preventive potential of GPC treatment on the brain irradiation-induced cytokine production in the peripheral circulation.…”

Можливості Фармакологічної Регуляції Енергетичного Метаболізму Мозку В ранньому Відновлювальному Періоді Інсульту

“…Основными направлениями лекарственной тера-пии в восстановительном периоде ИИ следует считать: 1) коррекцию артериального давления; 2) коррекцию реологических свойств крови; 3) стабилизацию тонуса мозговых сосудов; 4) нормализацию неврологического и когнитивно-го дефицита; 5) общеукрепляющую терапию и стимуляцию адаптационных возможностей организма [3,4,11,12,15,24,25].…”

New therapeutic and diagnostic approaches with which to influence mitochondrial dysfunctions

“…Furthermore, GPC, a water-soluble, deacylated PC derivative, proved to be effective against lipid peroxidation and loss of the membrane function in oxidoreductive injuries (Onishchenko, 2008). It has been shown to act via cholinergic pathways (Drago, 1992;Sigala, 1992) and has a stimulant effect on the growth hormone response too (Ceda, 1992).…”

“…It has been shown to act via cholinergic pathways (Drago, 1992;Sigala, 1992) and has a stimulant effect on the growth hormone response too (Ceda, 1992). GPC has been shown to be protective against membrane oxidation and can ameliorate the membrane function after traumatic injuries (Onischenko, 2008;Kidd, 2009). …”

“…GPC is a centrally-acting cholinergic precursor which increases the tolerance to ischemic tissue damage (Onishchenko, 2008 (Bauernschmitt, 1993;Lee, 1993;Amenta, 1994).…”