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ginkgolide/infarkt

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Strana 1 od 38 výsledky

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
Endoplasmic reticulum (ER) stress is increasingly recognized as an important causal factor of many diseases. Targeting ER stress has now emerged as a new therapeutic strategy for treating cardiovascular diseases. Here, we investigated the effects and underlying mechanism of ginkgolide K

Evaluation of in vitro inhibition and induction of cytochrome P450 activities by hydrolyzed ginkgolides.

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UNASSIGNED The extracts of Ginkgo biloba leaves are effective in treating cerebral infarction, of which ginkgolides have been demonstrated to be the active ingredients. The purpose of this study was to determine whether hydrolyzed ginkgolides would cause potential drug-drug interactions (DDI) during
We have previously reported that ginkgolides containing ginkgolides A and B (GKAB) reduce infarct size in a rat model of focal ischemia. c-Jun N-terminal kinase (JNK), also known as stress-activated kinase (SAPK), is a critical stress-responsive kinase activated by various brain insults. Previous
Ginkgolides (GG), containing ginkgolide A (GA), ginkgolide B (GB) and ginkgolide C (GC), are mainly prescribed for ischemic stroke and cerebral infarction. However, the ginkgolides can hardly pass the blood-brain barrier (BBB) into the brain. The purpose of this study was to prepare borneol-modified

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

[Effects of ginkgolide K on platelet aggregation activity and neuroprotection].

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To investigate the antagonism effects of different concentrations of ginkgolide K(GK) on platelet activating factor (PAF)-induced platelet aggregation and neuroprotective effect on cells and animal models of ischemia-reperfusion injury. GK-containing serum in rabbit was prepared, and the effects of

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

Ginkgolide C Alleviates Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Inhibition of CD40-NF-κB Pathway.

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Increasing evidence shows that inflammation plays a vital role in the occurrence and development of ischemia/reperfusion (I/R). Suppression of excessive inflammation can ameliorate impaired cardiac function, which shows therapeutic potential for clinical treatment of myocardial ischemia/reperfusion

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

[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
Cerebral ischemia-reperfusion (I/R) injury usually contributes to mortality and disability after ischemic stroke. Ginkgolides injection (GIn), a standard preparation composed of ginkgo diterpene lactones extract, is clinically used for neuroprotective treatment on reconvalescents of cerebral
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