ginkgolide b/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

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

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,

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

Ginkgolide B preconditioning protects neurons against ischaemia-induced apoptosis.

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Ischaemic preconditioning (IP) has been reported to protect the brain against subsequent lethal ischaemia, but it has not been used clinically to prevent ischaemic injury because of safety concerns. The aim of the present study was to see whether Ginkgolide B (GB) is capable of preconditioning as IP

Effects of Chinese herbal monomers on oxidative phosphorylation and membrane potential in cerebral mitochondria isolated from hypoxia-exposed rats in vitro.

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Mitochondrial dysfunction is the key pathogenic mechanism of cerebral injury induced by high-altitude hypoxia. Some Chinese herbal monomers may exert anti-hypoxic effects through enhancing the efficiency of oxidative phosphorylation. In this study, effects of 10 kinds of Chinese herbal monomers on

Protective effect of ginkgolide B on high altitude cerebral edema of rats.

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Ginkgolide B (GB) is one of the ginkgolides isolated from leaves of the Ginkgo biloba tree. The aim of this study was to investigate whether GB has a protective effect on high altitude cerebral edema (HACE) of rats. HACE was induced by hypobaric hypoxia exposure for 24 hours in an animal

Blood brain barrier permeability and therapeutic time window of Ginkgolide B in ischemia-reperfusion injury.

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The goal of this study was to estimate the blood brain barrier (BBB) permeability of Ginkgolide B in normal condition and models of ischemia both in vivo and in vitro. A sensitive LC-MS/MS analytical method was developed to determinate accurately the concentration of Ginkgolide B in cell, plasma and

The combined effects of ginkgo biloba extracts and aspirin on viability of sk-N-mc, neuroblastoma cell line in hypoxia and reperfusion condition.

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OBJECTIVE The purpose of this study is to investigate the combined effects of ginkgo biloba extract, ginkgolide A and B and aspirin on SK-N-MC, human neuroblastoma cell viability and mRNA expression of growth associated protein43 (GAP43), Microtubule-associated protein 2 (MAP2), B-cell lymphoma2

Cardioprotection of Ginkgolide B on Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Regulation of A20-NF-κB Pathway.

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Inflammation urges most of the characteristics of plaques involved in the pathogenesis of myocardial ischemia/reperfusion injury (MI/RI). In addition, inflammatory signaling pathways not only mediate the properties of plaques that precipitate ischemia/reperfusion (I/R) but also influence the

Effect of ginkgolide B on striatal extracellular amino acids in middle cerebral artery occluded rats.

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BACKGROUND Ginkgo biloba leaves are traditionally used in China for its health-promoting properties. There is substantial experimental evidence to support the view that Ginkgo biloba extracts have neuroprotective properties under conditions such as hypoxia/ischemia. Although a number of studies have

The CNS effects of Ginkgo biloba extracts and ginkgolide B.

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Ginkgo biloba extracts such as EGb-761 have been suggested to have a multitude of beneficial effects on CNS function, from enhancing cognitive function in dementia to facilitating recovery from acute forms of neural damage such as hypoxia/ischemia. Ginkgolide B, one of the major components of

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