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ginkgolide b/infarto
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 26 risultati
Ginkgolide B attenuates myocardial infarction-induced depression-like behaviors via repressing IL-1β in central nervous system
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Depression is common in patients with myocardial infarction (MI), attributing to worse outcomes. Inflammatory response in the central nervous system (CNS) is considered to be a potential mechanism underlying MI induced depression. Our former research demonstrated Ginkgo biloba extract played an
Ginkgolide B for Myocardial Ischemia/Reperfusion Injury: A Preclinical Systematic Review and Meta-Analysis.
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Ginkgolide B (GB) is an extract of dried Ginkgo biloba leaves and possesses various pharmacological activities in the cardiovascular system. Herein, we aim to assess the available preclinical evidence and possible mechanisms of GB for myocardial ischemia/reperfusion injury. The study quality score
[Effects of Ginkgolide B on inflammation induced by cerebral ischemia-reperfusion in rats].
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OBJECTIVE
To investigate the protective effects of Ginkgolide B on inflammation induced by cerebral ischemia-reperfusion in rats.
METHODS
Rats were pretreated with Ginkgolide B at the dose of 2. 5, 5, 10 mg/kg for 3 days and then subjected to cerebral ischemia/reperfusion induced by a middle
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
Ginkgolide B Modulates BDNF Expression in Acute Ischemic Stroke.
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OBJECTIVE
To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned.
METHODS
Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation
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
Improvement of contractile function in isolated cardiomyocytes from ischemia-reperfusion rats by ginkgolide B pretreatment.
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Ginkgo biloba extract is an important natural product for treatment of cerebral and cardiovascular diseases, whereas ginkgolide B (GB) is a main component of it. Its effects on ischemic heart and ventricular contractile function in Sprague-Dawley male rats are unclear yet. In the present study, we
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
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
Different neuroprotective responses of Ginkgolide B and bilobalide, the two Ginkgo components, in ischemic rats with hyperglycemia.
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Ginkgo biloba extracts show neuroprotective effects during cerebral ischemia, but with various components, the mechanisms of action remain unclear. In this study, we tested the effects of Ginkgolide B (GB) and bilobalide (BB) on normoglycemic and hyperglycemic rats subjected to transient cerebral
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
[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
Neuroprotective effects of NV-31, a bilobalide-derived compound: evidence for an antioxidative mechanism.
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In previous studies we have already shown that the extract of Ginkgo biloba, and some of its constituents, such as ginkgolide B and bilobalide, protected cultured neurons against apoptotic and excitotoxic damage and reduced the infarct volume after focal cerebral ischemia in mice and rats. In this
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