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n butylphthalide/infarci
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3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK.
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Influence of dl-3-N-butylphthalide on infarction size in rats with acute myocardial infarction
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Objective: To study the influence of dl-3-N-butylphthalide (NBP) on infarction size in rats with acute myocardial infarction (AMI).
Methods: AMI model was established by
Effects of dl-3-n-butylphthalide on serum lipoprotein-associated phospholipase A2 and hypersensitive C-reactive protein levels in acute cerebral infarction.
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Use of l-3-n-Butylphthalide within 24 h after intravenous thrombolysis for acute cerebral infarction
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Objective: Observe the clinical efficacy of l-3-n-Butylphthalide (NBP) in acute ischemic stroke (AIS) patients within 24 h after intravenous thrombolysis using recombinant tissue plasminogen activator (hereafter termed "IT").
Effects of dl-3-n-butylphthalide on serum VEGF and bFGF levels in acute cerebral infarction.
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OBJECTIVE
To observe the curative effect of dl-3-n-Butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on levels of serum vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).
METHODS
A total of 160 ACI patients treated in our hospital
Dl-3-n-butylphthalide protects the blood brain barrier of cerebral infarction by activating the Nrf-2/HO-1 signaling pathway in mice.
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OBJECTIVE
The aim of this study was to explore whether Dl-3-n-butylphthalide (DBT) could protect blood-brain barrier (BBB) of mice with experimental cerebral infarction and the relevant mechanism.
METHODS
Adult male CD-1 mice were selected as the study objects. The permanent middle cerebral artery
Effects of Dl-3-n-butylphthalide on Cerebral Ischemia Infarction in Rat Model by Mass Spectrometry Imaging.
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Dl-3-n-butylphthalide (NBP) is a drug that is used in the treatment of ischaemic stroke. However, to the best of our knowledge, there are no systematic studies investigating the effects of dl-3-n-butylphtalide on the brain metabolism of small molecules. In this study, we first investigated the
2-(1-Hydroxypentyl)-benzoate increases cerebral blood flow and reduces infarct volume in rats model of transient focal cerebral ischemia.
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2-(1-Hydroxypentyl)-benzoate (dl-PHPB), a derivate of 3-n-butylphthalide (dl-NBP), is a novel drug candidate used for treatment of cerebral ischemia. The goal of the present study was to investigate the effects of dl-PHPB on infarct volume, neurological function, and cerebral blood flow (CBF) in
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
[Effect of dl-3-n-butylphthalide on delayed neuronal damage after focal cerebral ischemia and intrasynaptosomes calcium in rats].
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Effect of dl-3-n-butylphthalide on the size of infarction and behavior changes were investigated after delayed neuronal damage in rats subjected to permanent middle cerebral artery occlusion (MCAO) by the method of Tamura et al, and the scores of behavior were evaluated by the method of Bederson et
[Protective effect of dl-3-n-butylphthalide on ischemic neurological damage and abnormal behavior in rats subjected to focal ischemia].
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dl-3-n-Butylphthalide (NBP) was known to have improving effect on brain energy metabolism after ischemia insult. The purpose of this study is to determine if the drug has protective action against ischemic neuronal damage. In the present study, the effect of NBP on cerebral infarction and
DL-3-n-Butylphthalide, an anti-oxidant agent, prevents neurological deficits and cerebral injury following stroke per functional analysis, magnetic resonance imaging and histological assessment.
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DL-3-n-Butylphthalide (NBP) is a synthetic compound based on L-3-n-Butylphthalide which was isolated from seeds of Apium graveolens. The present study aims at evaluating the outcome of NBP given prior to and after the onset of ischemic stroke in spontaneously hypertensive rats (SHR) and normotensive
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,
Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury via ERK Signaling.
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UNASSIGNED
The aim of this study was to explore the role of DL-3-n-butylphthalide (NBP) in cerebral ischemia-reperfusion injury (CIRI) mice model. The involvement of extracellular signal-regulated kinase (ERK) signaling pathway was also investigated.
UNASSIGNED
All mice were divided into five
Discovery of a ring-opened derivative of 3-n-butylphthalide bearing NO/H2S-donating moieties as a potential anti-ischemic stroke agent.
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To search for novel anti-ischemic stroke agents with higher potency than a known drug 3-n-butylphthalide (NBP), a series of ring-opened derivatives of NBP bearing both nitric oxide (NO) and hydrogen sulfide (H2S)-donating moieties (NO/H2S-NBP) (8a-8o) were designed, synthesized, and biologically
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