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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

[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

Therapeutic neuroprotective effects of ginkgolide B on cortex and basal ganglia in a rat model of transient focal ischemia.

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Cerebral ischemia and reperfusion is one of the leading causes for death and severe disabilities in the world and often lead to irreversible brain damage over later lifespan. The aim of this study was to investigate the evolution of pathological damage in cerebral cortex and basal ganglia following

Improving effect of Ginkgolide B on mitochondrial respiration of ischemic neuron after cerebral thrombosis in tree shrewa.

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BACKGROUND It has been known that platelet activating factor receptors (PAFR) may mediate many acute pathological responses and that PAFR antagonist Ginkgolide B (GB) possesses multiple effects, but the actions of GB on PAFR affinity and mitochondrial respiration in the ischemic neuron were unclear

Ginkgolide B ameliorates NLRP3 inflammasome activation after hypoxic-ischemic brain injury in the neonatal male rat.

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BACKGROUND Perinatal hypoxic-ischemic (HI) insult is an important cause of brain injury in neonates. The development of novel treatment strategies for neonates with HI brain injury is urgently needed. Ginkgolide B (GB) is a main component of Ginkgo biloba extracts with a long history of use in

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

Induction of mast cell accumulation, histamine release and skin edema by N49 phospholipase A2.

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BACKGROUND It has been recognized that phospholipase A2 (PLA2) is a crucial component of snake venom, which contributes greatly to snake venom induced inflammation in man. However, the mechanisms through which N49 PLA2 provoke inflammation remain unclear. Recently, a N49 PLA2, TM-N49 from

Inhibition of NF-κB activation is associated with anti-inflammatory and anti-apoptotic effects of Ginkgolide B in a mouse model of cerebral ischemia/reperfusion injury.

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Ginkgolide B (GB) has potent neuroprotective effects against ischemia-induced brain injury in vivo and in vitro. However, the underlying mechanisms of GB's neuroprotection remain poorly understood. Excessive inflammation and apoptosis contribute to the pathogenesis of ischemic brain damage, and

Role of nitric oxide in blood-brain barrier permeability, brain edema and cell damage following hyperthermic brain injury. An experimental study using EGB-761 and Gingkolide B pretreatment in the rat.

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The role of oxidative stress in hyperthermia induced upregulation of constitutive and inducible isoforms of nitric oxide synthase (NOS) in the central nervous system (CNS) was investigated using immunohistochemistry in a rat model. Exposure of rats to heat stress at 38 degrees C for 4 h resulted in

[Effect of compatibility of ginkgolide A, ginkgolide B and ginkgolide K].

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To investigate the best active compatibility of ginkgolide A, B and K (GA，GB，GK). The effects of GA, GB, GK alone, combinations of each two of them, and combinations of these three components on platelet-activating factor (PAF)-induced platelet aggregation activity and rat cerebral ischemia

Attenuated Blood-Brain Barrier Dysfunction by XQ-1H Following Ischemic Stroke in Hyperlipidemic Rats.

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Following ischemic stroke, blood-brain barrier (BBB) is disrupted and is further aggravated with the corresponding incidence of hyperlipidemia. BBB breakdown promotes inflammation infiltration into the brain, which exacerbates cerebral ischemic injury as a result. Here, we report that

XQ-1H protects against ischemic stroke by regulating microglia polarization through PPARγ pathway in mice.

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Cerebral ischemic and reperfusion injury often accompany with inflammation, and lead to severe neuronal damage, which further result in neurological disorders and memory disorders. In this study, we researched XQ-1H, a novel derivative of ginkgolide B, protecting against ischemic stroke in mice

The neuroprotective mechanisms of ginkgolides and bilobalide in cerebral ischemic injury: a literature review.

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The incidence and mortality of strokes have increased over the past three decades in China. Ischemic strokes can cause a sequence of detrimental events in patients, including increased permeability and dysfunction of the blood-brain barrier, brain edema, metabolic disturbance, endoplasmic reticulum

Pharmacokinetics and pharmacodynamics analysis of XQ-1H and its combination therapy with clopidogrel on cerebral ischemic reperfusion injury in rats.

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Ischemic stroke is the main cause of disability and mortality worldwide. 10-O-(N N-dimethylaminoethyl)-ginkgolide B methane-sulfonate (XQ-1 H) is a novel drug based on the remedial approach for ischemic stroke. Clopidogrel, a widely used anti-platelet drug, is often co-prescribed in the clinic. In

XQ-1H Suppresses Neutrophils Infiltration and Oxidative Stress Induced by Cerebral Ischemia Injury Both In Vivo and In Vitro.

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Cerebral ischemia/reperfusion injury plays an important role in the development of tissue injury after acute stroke, including neutrophils adhesion and infiltration, inflammation and oxidative stress. 10-O-(N,N-dimethylaminoethyl)-ginkgolide B methanesulfonate (XQ-1H) is a novel ginkdolide B

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