Magnesium sulfate protects blood–brain barrier integrity and reduces brain edema after acute ischemic stroke in rats

Shadman, Javad; Sadeghian, Nooshin; Moradi, Alireza; Bohlooli, Shahab; Panahpour, Hamdollah

doi:10.1007/s11011-019-00419-y

Cited by 32 publications

(17 citation statements)

References 38 publications

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“…Intraperitoneal injections with magnesium sulfate in normal mice reduced histamine-induced endothelial hyper-permeability mainly by suppressing oxidative stress and inflammatory responses, while up-regulating endothelial barrier-stabilizing mediators such as cyclic adenosine monophosphate ( 7 ). In rats subjected to transient focal cerebral ischemia, magnesium showed the ability to protect BBB integrity by increasing the activity of anti-oxidant enzymes and decreasing lipid peroxide levels ( 9 ). Another pivotal pathogenesis of HT after IVT is rt-PA induced coagulopathy ( 2 , 21 ).…”

Section: Discussionmentioning

confidence: 99%

“…This is different from the positive findings that serum magnesium levels affect the risk of HT after thrombolysis. A reasonable explanation is that low serum magnesium levels are associated with larger infarct volume ( 9 , 29 ). Thus, subsequent hemorrhage in ischemic lesions are not sufficient to cause further deterioration of neurological function.…”

Section: Discussionmentioning

confidence: 99%

“…Brain microvascular endothelium is the fundamental component of BBB and the initiation of ischemia-related BBB disruption is predominantly triggered by endothelial damage ( 8 ). Recent evidence indicates the protective effect of magnesium on BBB in rats with transient focal cerebral ischemia ( 9 ). In addition, magnesium is involved in the coagulation cascade ( 10 , 11 ) and platelet activation ( 12 ); magnesium deficiency would lead to dysfunction of coagulation system.…”

Section: Introductionmentioning

confidence: 99%

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Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke

et al. 2020

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Background: In patients with acute ischemic stroke, hemorrhagic transformation is a major complication after intravenous thrombolysis. This study aimed to investigate the relationship between serum magnesium levels and hemorrhagic transformation (HT) after thrombolytic therapy. Methods: We retrospectively analyzed data from 242 patients who received thrombolytic therapy at the Second Affiliated Hospital of the Wenzhou Medical University in China. Baseline serum magnesium levels were measured before intravenous thrombolysis, and the occurrence of HT was evaluated using computed tomography images reviewed within 24–36 h after therapy. The relationship between serum magnesium levels and HT was examined using multivariate logistic regression, subgroup analysis, and restricted cubic spline models. Results: Of the 242 included patients, 43 (17.8%) developed HT. Patients with HT had significant lower serum magnesium levels than those without HT (0.81 ± 0.08 vs. 0.85 ± 0.08 mmol/L, p = 0.007). Multivariable logistic regression analysis indicated that patients with higher serum magnesium levels had lower risk of HT (OR per 0.1-mmol/L increase 0.43, 95% CI 0.27–0.73, p = 0.002). However, this association did not persist when baseline levels of serum magnesium were higher than the median value (0.85 mmol/L) in subgroup analysis (OR per 0.1-mmol/L increase 0.58, 95% CI 0.14–2.51, p = 0.47). This threshold effect was also observed in the restricted cubic spline model when serum magnesium levels were above 0.88 mmol/L. No association between symptomatic HT and serum magnesium levels was observed in our study (OR per 0.1-mmol/L increase 0.52, 95% CI 0.25–1.11, p = 0.092). Conclusions: Lower serum magnesium levels in patients with ischemic stroke are associated with an increased risk of HT after intravenous thrombolysis, but perhaps only when serum magnesium is below a certain minimal concentration.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke

et al. 2020

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“…In addition it has been reported that magnesium could show cholinomimetic effects and improve the cholinergic pathways activities [34]. There are evidences which illustrated Magnesium stabilizes the blood brain barrier and increases its integrity [35]. The last mechanism could limit the aluminum access to the central nervous system.…”

Section: Discussionmentioning

confidence: 99%

Magnesium Increases the Protective Effect of Citicoline on Aluminum Chloride-induced Cognitive Impairment

Hosseini-Sharifabad

Rabbani

Seyed-Yousefi

et al. 2020

Clin Psychopharmacol Neurosci

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Objective: Alzheimer's disease is a popular neurodegenerative disorder which is growing in the elderly people. Exposure to environmental pollutant like aluminum could trigger or accelerate its involved mechanisms like tau phosphorylation. The current study will evaluate the effect of alone or co-administration of Citicoline or/and magnesium on the aluminum chloride induced memory impairment. Methods: Male albino mice were randomly divided into different groups (n = 7). Memory impairment was induced via orally administration of 300 mg/kg Aluminum Chloride for 28 days. Based on respective group, animals received 100, 250, 500 mg/kg of Citicoline or 50, 100, 150 mg/kg of Magnesium sulfate (MgSO4), intraperitoneally. In co-administration, 50 mg/kg of MgSO4 injected concomitantly with 100, 250, or 500 mg/kg of Citicoline. Rivastigmine (2 mg/kg intraperitoneally) was used as a positive control. Memory was evaluated using the Object Recognition Task (ORT) and Passive Avoidance Test (PAT). Results: The studied doses of Citicoline or MgSO4 when administered individually showed significant increase in the discrimination index in ORT and latency time in the PAT compared to the Aluminium chloride (AlCl3) treated group. Concomitant injection of 50 mg/kg MgSO4 with the different doses of Citicoline strongly increased the above indices values in comparison to each alone. Conclusion: The findings show, individual administration of Citicoline or MgSO4 inverted the AlCl3-induced memory impairment in a dose independent manner. The addition of MgSO4 to the Citicoline showed a synergistic effect in the PAT and likely additive effect in the ORT.

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“…Magnesium sulfate has been investigated as a calcium channel blocker, as well as an anticonvulsant, a cardiovascular drug, an anesthetic, a tocolytic agent, an anti-arrhythmia drug, and an analgesic (PubChem CID: 24083). Magnesium sulfate has shown neuroprotective effect post-stroke in several animal models ( 50 – 53 ). However, a randomized clinical trial in stroke patients showed no overall benefit when magnesium sulfate was administered at times of ~7.5 h after stroke symptom onset (NCT01502761).…”

Section: Strokementioning

confidence: 99%

Anti-inflammatory and Neuroprotective Agents in Clinical Trials for CNS Disease and Injury: Where Do We Go From Here?

et al. 2020

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Neurological disorders are major contributors to death and disability worldwide. The pathology of injuries and disease processes includes a cascade of events that often involve molecular and cellular components of the immune system and their interaction with cells and structures within the central nervous system. Because of this, there has been great interest in developing neuroprotective therapeutic approaches that target neuroinflammatory pathways. Several neuroprotective anti-inflammatory agents have been investigated in clinical trials for a variety of neurological diseases and injuries, but to date the results from the great majority of these trials has been disappointing. There nevertheless remains great interest in the development of neuroprotective strategies in this arena. With this in mind, the complement system is being increasingly discussed as an attractive therapeutic target for treating brain injury and neurodegenerative conditions, due to emerging data supporting a pivotal role for complement in promoting multiple downstream activities that promote neuroinflammation and degeneration. As we move forward in testing additional neuroprotective and immune-modulating agents, we believe it will be useful to review past trials and discuss potential factors that may have contributed to failure, which will assist with future agent selection and trial design, including for complement inhibitors. In this context, we also discuss inhibition of the complement system as a potential neuroprotective strategy for neuropathologies of the central nervous system.

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Magnesium sulfate protects blood–brain barrier integrity and reduces brain edema after acute ischemic stroke in rats

Cited by 32 publications

References 38 publications

Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke

Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke

Magnesium Increases the Protective Effect of Citicoline on Aluminum Chloride-induced Cognitive Impairment

Anti-inflammatory and Neuroprotective Agents in Clinical Trials for CNS Disease and Injury: Where Do We Go From Here?

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