Methylene blue and normobaric hyperoxia combination therapy in experimental ischemic stroke

Rodriguez, Pavel; Zhao, Jiang; Milman, Brian; Tiwari, Yash; Duong, Timothy Q.

doi:10.1002/brb3.478

Cited by 13 publications

(6 citation statements)

References 53 publications

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“…A novel example of this combined normobaric hyperoxia treatment with MB. Combination therapy decreased infarct volume and yielded behavioral improvements in a stroke model beyond that of either treatment alone [56]. Our work found that the addition of MB to therapeutic hypothermia managed to rescue neuronal cell death and behavioral outcomes after extended GCI.…”

Section: Methylene Blue Mitochondrial Dysfunction and Neurodegenementioning

confidence: 79%

From Mitochondrial Function to Neuroprotection—an Emerging Role for Methylene Blue

2017

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Methylene blue (MB) is a well-established drug with a long history of use, owing to its diverse range of use and its minimal side effect profile. MB has been used classically for the treatment of malaria, methemoglobinemia, and carbon monoxide poisoning, as well as a histological dye. Its role in the mitochondria, however, has elicited much of its renewed interest in recent years. MB can reroute electrons in the mitochondrial electron transfer chain directly from NADH to cytochrome c, increasing the activity of complex IV and effectively promoting mitochondrial activity while mitigating oxidative stress. In addition to its beneficial effect on mitochondrial protection, MB is also known to have robust effects in mitigating neuroinflammation. Mitochondrial dysfunction has been identified as a seemingly unifying pathological phenomenon across a wide range of neurodegenerative disorders, which thus positions methylene blue as a promising therapeutic. In both in vitro and in vivo studies, MB has shown impressive efficacy in mitigating neurodegeneration and the accompanying behavioral phenotypes in animal models for such conditions as stroke, global cerebral ischemia, Alzheimer's disease, Parkinson's disease, and traumatic brain injury. This review summarizes recent work establishing MB as a promising candidate for neuroprotection, with particular emphasis on the contribution of mitochondrial function to neural health. Furthermore, this review will briefly examine the link between MB, neurogenesis, and improved cognition in respect to age-related cognitive decline.

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Section: Methylene Blue Mitochondrial Dysfunction and Neurodegenementioning

confidence: 79%

From Mitochondrial Function to Neuroprotection—an Emerging Role for Methylene Blue

2017

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“…The foot fault score of the foot fault test was determined to evaluate walking ability at 41 days after induction brain inflammation, as described previously (Rodriguez et al, 2016). The rat was placed on an elevated, grid floor (34 mm×29 mm) for 2 min.…”

Section: Methodsmentioning

confidence: 99%

Treadmill exercise and wheel exercise improve motor function by suppressing apoptotic neuronal cell death in brain inflammation rats

Song

Jee

et al. 2018

J Exerc Rehabil

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Brain inflammation is involved in many brain disorders, such as brain ischemic injury, Alzheimer diseases, and Parkinson disease. Physical exercise has been recommended for the prevention and treatment of many brain inflammatory diseases. In the present study, the effects of exercise on motor function in relation with apoptotic neuronal cell death following neuroinflammation were investigated. Moreover, we compared the effect of forced exercise with voluntary exercise on neuroinflammation-induced motor malfunction. For this study, rota-rod test, vertical pole test, foot fault test, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, immunohistochemistry for caspase-3, and western blot for Bcl-2 and Bax were performed. Lipopolysaccharide was intraventricular infused for induction of brain inflammation. Treadmill exercise and wheel exercise were conducted during 6 weeks. In the present results, Treadmill exercise and wheel exercise alleviated brain inflammation-induced motor impairments by suppressing apoptotic neuronal cell death in the motor cortex. These effects of treadmill exercise and wheel exercise were similarly appeared.

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“…For example, recent studies showed that NBO extended neuro-and vaso-protection of N-acetylcysteine in transient focal ischemia (Liu et al, 2016), combination of NBO and melatonin demonstrated more protective effect on reperfusion injury through regulation cerebral microcirculation (Beker et al, 2015). In addition, combination therapy of NBO with methylene blue improved functional outcome and reduced infarct volume compared to either treatment alone and these improvements extended up to 28 days (Rodriguez et al, 2016).…”

Section: Combination Treatment With Nbomentioning

confidence: 99%

Oxygen or cooling, to make a decision after acute ischemia stroke

Liu

Jin

2016

Med Gas Res

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The presence of a salvageable penumbra, a region of ischemic brain tissue with sufficient energy for short-term survival, has been widely agreed as the premise for thrombolytic therapy with tissue plasminogen activator (tPA), which remains the only United States Food and Drug Administration (FDA) approved treatment for acute ischemia stroke. However, the use of tPA has been profoundly constrained due to its narrow therapeutic time window and the increased risk of potentially deadly hemorrhagic transformation (HT). Blood brain barrier (BBB) damage within the thrombolytic time window is an indicator for tPA-induced HT and both normobaric hyperoxia (NBO) and hypothermia have been shown to protect the BBB from ischemia/reperfusion injury. Therefore, providing the O2 as soon as possible (NBO treatment), freezing the brain (hypothermia treatment) to slow down ischemia-induced BBB damage or their combined use may extend the time window for the treatment of tPA. In this review, we summarize the protective effects of NBO, hypothermia or their use combined with tPA on ischemia stroke, based on which, the combination of NBO and hypothermia may be an ideal early stroke treatment to preserve the ischemic penumbra. Given this, there is an urge for large randomized controlled trials to address the effect.

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Methylene blue and normobaric hyperoxia combination therapy in experimental ischemic stroke

Cited by 13 publications

References 53 publications

From Mitochondrial Function to Neuroprotection—an Emerging Role for Methylene Blue

From Mitochondrial Function to Neuroprotection—an Emerging Role for Methylene Blue

Treadmill exercise and wheel exercise improve motor function by suppressing apoptotic neuronal cell death in brain inflammation rats

Oxygen or cooling, to make a decision after acute ischemia stroke

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