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").
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
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
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 (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 (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 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
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 (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
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,
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
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