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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 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
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
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
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
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
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
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,
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
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
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
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
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
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