Evaluating the Efficacy of Citicoline in Embolic Ischemic Stroke in Rats: Neuroprotective Effects When Used Alone or in Combination with Urokinase

Shuaib, Ashfaq; Yang, Yi; Li, Qiu

doi:10.1006/exnr.1999.7314

Cited by 58 publications

(37 citation statements)

References 44 publications

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“…Application of citicoline, a neuroprotective substance (Shuaib et al, 2000), on the other hand, was ineffective ( Fig. 6a; n ϭ 6, p Ͻ 0.05), suggesting that certain, as yet unidentified, forms of cell damage do not appear to occur.…”

Section: Resultsmentioning

confidence: 99%

“…Second, histological analysis after transient hypoxic episodes revealed no evidence of cellular damage. Third, the ineffectiveness of citicoline (Shuaib et al, 2000) further suggests that certain, as yet unidentified, forms of cell damage do not appear to occur. Nevertheless, the functional interruption seems to be specific, since average swim speed was not affected.…”

Section: Discussionmentioning

confidence: 99%

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Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Sun

Xu²,

Alkon³

2002

J Pharmacol Exp Ther

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Hypoxia significantly reduced cholinergic activity in rat CA1 field and intracellular in the CA1 pyramidal cells, recorded in hippocampal slices. The hypoxic responses of the hippocampal CA1 pyramidal cells to a brief hypoxia consisted of a short period of "synaptic arrest", observed as an elimination of excitatory postsynaptic current under voltage clamp and recovered immediately as oxygenation was reinitiated. The hypoxic synaptic arrest was not associated with reduced postsynaptic responses of the pyramidal cells to externally applied L-glutamate, suggesting that the synaptic arrest might result from a presynaptic mechanism. The hypoxic synaptic arrest was abolished in the presence of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a specific adenosine A 1 receptor antagonist. Blocking adenosine A 1 receptors also eliminated effects of hypoxia on the hippocampal CA1 field activity and intracellular of the CA1 pyramidal cells. In behaving rats, brief hypoxia impaired their water maze performance in both the escape latency and probe tests. The impairment was prevented by intralateral cerebroventricular injections of DPCPX. These results suggest that hypoxia releases adenosine and produces an inhibition of synaptic transmission and intracellular signal cascade(s) involved in generation/maintenance of hippocampal CA1 activity. This protection of synaptic efficacy and spatial learning through adenosine A 1 receptor antagonism may represent an effective therapeutic strategy to eliminate functional interruption due to transient hypoxic episodes and/or chronic hypoxia secondary to compromise of respiratory function.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Sun

Xu²,

Alkon³

2002

J Pharmacol Exp Ther

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“…Изучена роль фосфолипидов при гемокоагуляции. Внутрисосудистое фибринообразование характеризуется расстройствами свертывающей системы крови с нарушением соотноше-ния между нейтральными (НФЛ) и кислыми фосфолипи-дами (КФЛ) [22]. Процесс трансформации фибриногена в фибрин, сопровождающийся уменьшением содержания КФЛ и возрастанием уровня НФЛ, изменяет это соотно-шение.…”

Section: препараты нейромедиаторного и нейрометаболического действияunclassified

Combined therapy of cerebrovascular disorders with neuroprotectors

Путилина¹

2016

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Комбинированное применение нейропротекторов в терапии цереброваскулярных заболеваний м.В. ПУТилина ФгБоУ Во «российский национальный исследовательский медицинский университет им. н.и. Пирогова», москва, россия лекарственная безопасность является одним из приоритетных направлений современной медицины. Задача медикаментозной терапии -не только поиск эффективных и безопасных препаратов, но и изучение возможности комбинированного применения препаратов с разнонаправленным нейропротективным действием. С учетом возможных лекарственных взаимодействий можно рекомендовать этилметилгидроксипиридина сукцинат как средство базовой терапии больных с цереброваскулярными заболеваниями для нормализации энергетического метаболизма клеток мозга. Эффективно комплексное введение холинергических препаратов с различными нейропротективными эффектами с первых часов пребывания больного в стационаре. Выбор первоочередного назначения холинергических препаратов (цитиколин или холина альфосцерат) должен быть обоснован с учетом нарушений функционирования систем активации головного мозга. Предикторами эффективности терапии являются возраст пациента, уровень сознания, наличие соматической патологии, перенесенные ранее инсульты, когнитивные нарушения. Ключевые слова: лекарственная безопасность, цитиколин, холина альфосцерат, этилметилгидроксипиридин сукцинат, лечение. Combined therapy of cerebrovascular disorders with neuroprotectors m.V. PuTiliNAPirogiv russian National research medical university, moscow, russia Safety of drugs is one of the priorities of modern medicine. The goal of pharmacological treatment is a search for effective and safety drugs as well as a study of possibilities of combined using of the drugs with opposite effects. Basing on the possible therapeutic interactions, 2-ethyl-6-methyl-3-hydroxypyridine succinate can be recommended as a basic medication for patients with cerebrovascular diseases to normalize the energy metabolism of brain cells. The complex use of cholinergic drugs with different neuroprotective effects is effective from the first hours after admission. Cholinergic drugs (citicoline or choline alfoscerate) as the drugs of the first choice should be justified taking into consideration dysfunction of the brain system activation. Patient's age, the level of consciousness, somatic pathology, previous strokes, cognitive impairment are predictors of treatment efficacy.

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“…Studies in animal models of ischemia and hypoxia report that citicoline decreases neurological deficits, and improves behavioral performance of learning and memory tasks [126]. There have also been preclinical studies reporting enhanced efficacy when citicoline was administered along with or following intravenous thrombolysis [127][128][129], and along with other potential neuroprotective therapies, such as mild hypothermia [130]. Multiple, randomized clinical stroke trials have investigated citicoline and reported that administration of citicoline was effective early in the post-ischemia recovery process, as demonstrated by improved level of consciousness [131], and improvements in the modified Rankin score [132].…”

Section: Citicolinementioning

confidence: 99%

Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

2011

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Stroke is one of the leading causes of death and disability worldwide. Current treatment strategies for ischemic stroke primarily focus on reducing the size of ischemic damage and rescuing dying cells early after occurrence. To date, intravenous recombinant tissue plasminogen activator is the only United States Food and Drug Administration approved therapy for acute ischemic stroke, but its use is limited by a narrow therapeutic window. The pathophysiology of stroke is complex and it involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis, neuroprotection, and neurorestoration. Regeneration of the brain after damage is still active days and even weeks after a stroke occurs, which might provide a second window for treatment. A huge number of neuroprotective agents have been designed to interrupt the ischemic cascade, but therapeutic trials of these agents have yet to show consistent benefit, despite successful preceding animal studies. Several agents of great promise are currently in the middle to late stages of the clinical trial setting and may emerge in routine practice in the near future. In this review, we highlight select pharmacologic and cell-based therapies that are currently in the clinical trial stage for stroke.

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Evaluating the Efficacy of Citicoline in Embolic Ischemic Stroke in Rats: Neuroprotective Effects When Used Alone or in Combination with Urokinase

Cited by 58 publications

References 44 publications

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Pharmacological Protection of Synaptic Function, Spatial Learning, and Memory from Transient Hypoxia in Rats

Combined therapy of cerebrovascular disorders with neuroprotectors

Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

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