Effect of repeatedly given CDP-choline on cardiovascular and tissue injury in spinal shock conditions: investigation of the acute phase

Coskun, Cenk; Avcı, Berrin; Ocak, Nihal; Yalçın, Murat; Dirican, Melahat; Savci, Vahide

doi:10.1211/jpp.62.04.0013

Cited by 13 publications

(10 citation statements)

References 30 publications

(42 reference statements)

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“…More recent evidences suggest that citicoline may increase dopamine production and glutamate uptake in the brain to improve cognition [2], [3]. Citicoline could also reduce free fatty acid release and recover the activities of mitochondrial ATPase and membrane Na + /K + ATPase to alleviate brain damage [4], [5].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia/Aglycemia-Induced Endothelial Barrier Dysfunction and Tight Junction Protein Downregulation Can Be Ameliorated by Citicoline

Zhang

Pan

et al. 2013

PLoS ONE

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This study explores the effect of citicoline on the permeability and expression of tight junction proteins (TJPs) in endothelial cells under hypoxia/aglycemia conditions. Hypoxia or oxygen and glucose deprivation (OGD) was utilized to induce endothelial barrier breakdown model on human umbilical vein endothelial cells (HUVECs) and mouse brain microvascular endothelial cells (bEnd.3s). The effect of citicoline on endothelial barrier breakdown models was determined at either low or high concentrations. FITC-Dextran flux was used to examine the endothelial permeability. The expression of TJPs was measured by immunofluorescence, Real-time PCR and Western Blot methods. Results showed that hypoxia or OGD increased the permeability of HUVECs accompanied with down-regulation of occludens-1 (ZO-1) and occludin at both mRNA and protein levels. Similarly in bEnd.3s, hypoxia increased the permeability and decreased the expression of ZO-1 and claudin-5. Citicoline treatment dose-dependently decreased the permeability in these two models, which paralleled with elevated expression of TJPs. The data demonstrate that citicoline restores the barrier function of endothelial cells compromised by hypoxia/aglycemia probably via up-regulating the expression of TJPs.

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Section: Introductionmentioning

confidence: 99%

Hypoxia/Aglycemia-Induced Endothelial Barrier Dysfunction and Tight Junction Protein Downregulation Can Be Ameliorated by Citicoline

Zhang

Pan

et al. 2013

PLoS ONE

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“…The activation of central cholinergic receptors through the increase in brain choline levels mediates these effects (32). We also reported that CDP-choline is able to decrease neuronal injury in spinal cord transected rats by limiting oxidative injury (11). Additionally, we demonstrated that intravenously given CDP-choline exposes intense coverage versus arrhythmias and increase survival rates in short-term ischemia-reperfusion of myocardium by activating efferent vagal pathways followed by increased brainstem cholinergic transmission throughout the initiation of central muscarinic receptors in rats (45).…”

Section: Introductionmentioning

confidence: 77%

“…CDP-choline-induced tissue protection may have been through i) the improved tissue perfusion due to drug's pressor effect, ii) the alleviation of inflammatory conditions due to the drug-induced decrease in plasma proinflammatory cytokins. CDP-choline also can reduce oxidative stress in several pathological conditions (3,11). Therefore the antioxidant effect of CDP-choline may have another explanation of its tissue protective effect.…”

Section: Discussionmentioning

confidence: 99%

“…CDP-choline that was injected at 3 rd hours after CLI increased blood pressure and reversed hypotension without affecting the heart rate changes. The dose of CDPcholine was chosen from our earlier experiments in which the drug was shown to exert both cardiovascular and tissue protective effects in several conditions (11,31,32,45). Our previous reports repeatedly demonstrated that CDPcholine, administered either intracerebroventricularly or intravenously, can affect blood pressure and exert pressor response in normal and hypotensive conditions (31,32).…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of CDP-choline on hypotension and tissue injury in septic shock model

ALTINBAŞ

2017

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Summary: CDP-choline is an endogen molecule and also a drug that is used in several trauma and ischemic conditions. It has been demonstrated that it improves the hemodynamic parameters in different shock models and prevents tissue damage in rats. The current study tested the effect of CDP-choline on hypotension, inflammation and tissue injury induced by septic shock model in rats. Twenty-four adult, male Spraque-Dawley rats, weighing 250-300 g were used. Septic shock was induced by cecal ligation-incision (CLI). CDP-choline (100 mg/kg) injected intravenously (i.v.) at the 180 th minute of the experiment. The animals were observed for 180 minutes after the injection, then blood and tissue samples were obtained for cytokine measurements and histological examinations, respectively. The cecal ligation-incision decreased arterial pressure and increased heart rate. Intravenous injection of CDP-choline reversed hypotension and increased arterial pressure up to control levels within the first 60 minutes without changing the increase in heart rate. The effect lasted for 3 hours. CDP-choline attenuated the increases in TNF-α, IL-1β and IL-6 levels in septic shock. Moreover, the drug exerted protective effects for the injury induced by septic shock in lungs, liver and kidney tissues; whereas this effect was not present on spleen. In conclusion, the present data suggested that intravenous CDP-choline administration can improve the deteriorations in hemodynamic and inflammatory parameters and can prevent the tissue injury in septic shock-induced by CLI in rats.

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“…The mechanisms of this reduced neural activity remain poorly understood. At the same time, although the existence of an acute period of spinal shock in rats has been reported after severe spinal contusions (Taccola et al, 2020b ) it is rarely the case immediately after complete surgical transection of the cord conducted under full anesthesia (Coskun et al, 2010 ). Our study demonstrates that spinal reflexes in response to single epidural pulses remain unaffected by spinal transection, similar to what has been reported in awake rats (Lavrov et al, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Selective Antagonism of A1 Adenosinergic Receptors Strengthens the Neuromodulation of the Sensorimotor Network During Epidural Spinal Stimulation

Taccola

Salazar

Apicella

et al. 2020

Front. Syst. Neurosci.

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Although epidural spinal stimulation (ESS) results in promising therapeutic effects in individuals with spinal cord injury (SCI), its potential to generate functional motor recovery varies between individuals and remains largely unclear. However, both preclinical and clinical studies indicate the capacity of electrical and pharmacological interventions to synergistically increase the engagement of spinal sensorimotor networks and regain motor function after SCI. This study explored whether selective pharmacological antagonism of the adenosine A1 receptor subtype synergizes with ESS, thereby increasing motor response. We hypothesized that selective pharmacological antagonism of A1 receptors during ESS would produce facilitatory effects in spinal sensorimotor networks detected as an increased amplitude of spinally-evoked motor potentials and sustained duration of ESS induced activity. Terminal experiments were performed in adult rats using trains of stereotyped pulses at 40 Hz delivered at L5 with the local administration to the cord of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). We demonstrated that ESS combined with the blockage of A1 receptors increased the magnitude of the endogenous modulation and postponed the decay of responses that occur during ESS alone. Although DPCPX significantly increased the yield of repetitive stimulation in intact spinal cords, the effects of A1 antagonism on motor evoked responses after an acute spinal transection was not detected. These studies support the future investigation of the optimal dosage, methods of delivery, and systemic effects of the synergistic application of A1 antagonists and spinal stimulation in the intact and injured spinal cord.

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Effect of repeatedly given CDP-choline on cardiovascular and tissue injury in spinal shock conditions: investigation of the acute phase

Cited by 13 publications

References 30 publications

Hypoxia/Aglycemia-Induced Endothelial Barrier Dysfunction and Tight Junction Protein Downregulation Can Be Ameliorated by Citicoline

Hypoxia/Aglycemia-Induced Endothelial Barrier Dysfunction and Tight Junction Protein Downregulation Can Be Ameliorated by Citicoline

Protective effect of CDP-choline on hypotension and tissue injury in septic shock model

Selective Antagonism of A1 Adenosinergic Receptors Strengthens the Neuromodulation of the Sensorimotor Network During Epidural Spinal Stimulation

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