ginkgolide/hypoxia

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Ginkgolides B alleviates hypoxia-induced PC-12 cell injury by up-regulation of PLK1.

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Finding novel agent for cerebral ischemia therapy is urgently required. In our present study, we aimed to investigate the regulatory mechanism of Ginkgolides B (GB) in hypoxia-injured PC-12 cells.PC-12 cells were exposed to hypoxia and administrated with

Oral administration of Ginkgolide B alleviates hypoxia-induced neuronal damage in rat hippocampus by inhibiting oxidative stress and apoptosis.

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Objectives

The aim of this study is to explore the potential neuroprotective effects of Ginkgolide B (GB), a main terpene lactone and active component in Ginkgo biloba, in hypoxia-induced neuronal damage, and to further investigate its possible

[The protective effects of ginkgolide B and hypoxic preconditioning against acute hypoxia injury in mice].

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OBJECTIVE To investigate the protective effects of ginkgolide B and hypoxic preconditioning against acute hypoxia injury in mice. METHODS Ordinary pressure acute hypoxia model in mice was adopted to observe the ethology, the duration of the death and the degree of brain edema. Meanwhile the

Ginkgolides mimic the effects of hypoxic preconditioning to protect C6 cells against ischemic injury by up-regulation of hypoxia-inducible factor-1 alpha and erythropoietin.

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Hypoxic preconditioning can play a significant neuroprotective role. However, it has not been employed clinically because of safety concerns. To find a safer preconditioning stimulus that is both practical and effective, we investigated whether ginkgolides are capable of preconditioning as hypoxia

Hypoxia-induced apoptosis of cardiomyocytes is restricted by ginkgolide B-downregulated microRNA-29.

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Ginkgolide B exerts a cardioprotective function against ischemia-caused apoptosis in myocardial infarction. Here we sought out to address a functional mechanism associated with microRNA-29 (miR-29). Rat cardiomyocytes (H9c2 cells) were cultured in ginkgolide B-conditioned medium prior to hypoxic

Ginkgolides protect PC12 cells against hypoxia-induced injury by p42/p44 MAPK pathway-dependent upregulation of HIF-1alpha expression and HIF-1DNA-binding activity.

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We hypothesized that the neuroprotective role of the standardized Ginkgo biloba (Ginkgoaceae) extract EGb 761 under hypoxic conditions might be associated with its function to increase HIF-1 activity based on the fact that oxygen availability is crucial for cellular metabolism and viability and that

[Effects of ginkgolide (Gin) on cerebral water content, Na+, K(+) -ATPase activity, MDA, lactic acid of rats during acute hypoxia condition].

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Effects of ginkgolide B on isobaric hypoxic pulmonary hypertension in rats.

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OBJECTIVE To evaluate the effects of Ginkgolide B, a specific platelet activating factor (PAF) antagonist, on hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling. METHODS Forty male Wistar rats were divided into 4 groups, receiving normal saline, Ginkgolide B, isobaric hypoxia

[Effects of ginkgolide B on isobaric hypoxic pulmonary hypertension in rats].

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We examined the effects of ginkgolide B (BN52021), a specific platelet activating factor (PAF) antagonist, on hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling. Chronic hypoxia can cause pulmonary hypertension and pulmonary vascular remodeling in rats. Treated with BN52021,

Protective effects of two constituents of Chinese herbs on spinal motor neurons from embryonic rats with hypoxia injury.

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Neuroprotective agents are becoming significant tools in the repair of central nervous system injuries. In this study, we determined whether ginkgolides (Gin, extract of GinkgoBiloba) and Acanthopanax senticosus saponins (ASS, flavonoids extracted from Acanthopanax herbal preparations) have

[Ginkgolides induced ischemic tolerance and its possible molecular mechanism: experiment with rat pheochromocytoma cell line PC12].

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OBJECTIVE To explore the ischemic tolerance induced by Ginkgolides in PC12 cells and its possible molecular mechanism. METHODS An ischemic model was developed in PC12 cell line with deprivation of oxygen-glucose (OGD). PC12 cells was randomly divided into four groups: 9 hours ischemia group, 1.5

[Effect of ginkgolides on gene expression of HIF-1alpha in primary cultured neurons].

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OBJECTIVE To study the effects of ginkgolides (Gin) on the expression of hypoxia inducible factor-1 (HIF-1alpha) in hypoxic/ischemic neurons. METHODS The gene expression of HIF-1alpha pretreated with or without Gin (37.5 microg/ml) was observed by RT-PCR on primary cultured cortical neurons in the

[Expression of HIF-1alpha induced by ginkgolides in primary cultured cortical neurons and the relationship with ERK signal pathway].

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OBJECTIVE To study the effects of ginkgolides (Gin) on the expression of hypoxia-inducible factor-1alpha (H1F-1alpha) in primary cultured cortical neurons treated with CoCl2 and the relationship with ERK signal pathway. METHODS We observed the effects of Gin (37.5 mg/L) on morphology and viability

Platelet-activating factor enhances the expression of nerve growth factor in normal human astrocytes under hypoxia.

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Nerve growth factor (NGF) is required for the survival of neurons. We have addressed the effect of platelet-activating factor (PAF), one of the mediators of ischemic injury of the brain, on NGF expression in astrocytes. Normal human astrocytes in culture were stimulated with PAF, and levels of NGF

Hypothermia attenuates protective effects of ginkgolides on astrocytes from ischemia/reperfusion injury.

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The neuroprotective roles of both hypothermia and ginkgolides have been well confirmed. We first examined whether hypothermia (32 or 28 degrees C) or ginkgolides have a protective effect on astrocytes against ischemia and reperfusion-induced injury. We demonstrated that ginkgolides, but not

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