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3-N-Butylphthalide mitigates high glucose-induced injury to Schwann cells: association with nitrosation and apoptosis.

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A high glucose state readily causes peripheral axon atrophy, demyelination, loss of nerve fiber function, and delayed regeneration. However, few studies have examined whether nitration is also critical for diabetic peripheral neuropathy. Therefore, this study investigated the effects of high glucose

Dl-3-n-butylphthalide attenuates hypoxic-ischemic brain injury through inhibiting endoplasmic reticulum stress-induced cell apoptosis and alleviating blood-brain barrier disruption in newborn rats

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Dl-3-n-butylphthalide (NBP) has been demonstrated to exert neuroprotective effects in experimental models and human patients. This study was performed to assess the therapeutic effects and the underlying molecular mechanisms of NBP in a neonatal hypoxic-ischemic rat model. The results showed that

DL-3-n-butylphthalide improves cerebral hypoperfusion in patients with large cerebral atherosclerotic stenosis: a single-center, randomized, double-blind, placebo-controlled study

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Background: DL-3-n-butylphthalide (NBP) was demonstrated to increase the cerebral blood flow (CBF) in the animal models, but there are no clinic studies to verify this. We aimed to explore the effect of NBP on improving cerebral

DL-3-n-Butylphthalide protects rat bone marrow stem cells against hydrogen peroxide-induced cell death through antioxidation and activation of PI3K-Akt pathway.

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Bone marrow stem cells (BMSCs) have been one of the most important cell sources for cell replacement therapy (CRT) in cerebral infarction. However, long-lasting oxidative stress during stroke, which plays an important role in neuron damage, deteriorates the microenvironment for cell survival,

DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis.

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Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease characterized by progressive muscular atrophy, paralysis and bulbar symptoms. Transgenic mice over-expressing human mutant Cu/Zn superoxide dismutase-1 (SOD1) mimicked the pathological phenotype of ALS. dl-3-n-butylphthalide

Dl-3-N-butylphthalide attenuates ischemic reperfusion injury by improving the function of cerebral artery and circulation.

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Dl-3-N-butylphthalide (NBP) is approved in China for the treatment of ischemic stroke. Previous studies have shown that NBP promotes recovery after stroke via multiple mechanisms. However, the effect of NBP on vascular function and thrombosis remains unclear. Here, we aim to study the effect of NBP

Dl-3-N-Butylphthalide Alleviates the Blood-Brain Barrier Permeability of Focal Cerebral Ischemia Reperfusion in Mice.

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Ischemic stroke occurs following arterial occlusion and subsequent blood flow cease, and restoration of blood supply by thrombolytic therapy may cause cerebral ischemic reperfusion (IR) injury resulting in breakdowns of blood-brain barrier (BBB). Dl-3-n-butylphthalide (NBP) is an extraction from

A novel alpha-lipoic acid-3-n-butylphthalide conjugate enhances protective effects against oxidative stress and 6-OHDA induced neuronal damage.

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Neurodegenerative diseases are irreversible conditions that result in progressive degeneration and death of nerve cells. Although the underlying mechanisms may vary, oxidative stress is considered to be one of the major causes of neuronal loss. Importantly, there are still no comprehensive

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