n butylphthalide/hypoxia

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[Protective effects of d-, l-, and dl-3-n-butylphthalide on neuronal damage induced by hypoxia/hypoglycemia in cultured rat cortical neurons].

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The effects of l-3-n-butylphthalide(l-NBP) and d-3-n-butylphthalide(d-NBP) on hypoxia/hypoglycemia-induced cytotoxicity in primary cultured rat cortical neurons were studied. l-NBP and d-NBP(1-100 mumol.L-1) were shown to inhibit hypoxia/hypoglycemia-induced LDH release, decrease the percent of cell

DL-3-n-butylphthalide protects the blood-brain barrier against ischemia/hypoxia injury via upregulation of tight junction proteins.

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The increased permeability of the blood-brain barrier (BBB) induced by ischemia/hypoxia is generally correlated with alteration of tight junctions (TJs). DL-3-n-butylphthalide (NBP) has been shown to exert neuroprotective effects after ischemic injury. However, few studies have

Hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury.

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Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation -induced hypoxia inducible factor-1α expression. In this

DL-3-n-butylphthalide protects endothelial cells against oxidative/nitrosative stress, mitochondrial damage and subsequent cell death after oxygen glucose deprivation in vitro.

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DL-3-n-butylphthalide (NBP) has been used for stroke treatment in China for years. Recently, we found that NBP can reduce the incidence of stroke and have protective action on cerebral microvessels, suggesting a direct action of NBP on endothelial cells. However, it is difficult to evaluate the

[Effects of d-3-n-butylphthalide and l-3-n-butylphthalide on extracellular no level and intracellular cGMP level in primary cultured rat cortical neurons].

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The effects of l-3-n-butylphthalide(l-NBP) and d-3-n-butylphthalide(d-NBP) on extracellular nitric oxide (NO) levels and intracellular cyclic GMP (cGMP) levels were studied in primary cultured rat cortical neuronal cells. Nitric oxide and cGMP levels were measured by using spectrometry and

L-3-n-Butylphthalide protects rats' cardiomyocytes from ischaemia/reperfusion-induced apoptosis by affecting the mitochondrial apoptosis pathway.

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OBJECTIVE This study investigated the role of L-3-n-Butylphthalide (NBP) in cardiac protection. METHODS The left anterior descending coronary arteries (LAD) of the rats were occluded for 30 min following by 2-h reperfusion to make the ischaemia/reperfusion models. Neonatal cardiomyocytes were

Dl-NBP (Dl-3-N-Butylphthalide) Treatment Promotes Neurological Functional Recovery Accompanied by the Upregulation of White Matter Integrity and HIF-1α/VEGF/Notch/Dll4 Expression.

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Dl-3-n-butylphthalide (dl-NBP) was approved by the FDA of China for the treatment of acute ischemic stroke. Dl-NBP has been shown to promote neurological functional recovery and enhance white matter integrity using an endothelin-1-induced focal permanent cerebral ischemia model, which could mimic

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