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Страница 1 от 50 полученные результаты
Protection of vascular endothelial cells injured by angiotensin II and hypoxia in vitro by Ginkgo biloba (Ginaton).
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The objective of this study was to explore the protective effect and the possible mechanism of Ginkgo biloba extract (Ginaton) on human vascular endothelial cells (VECs) injured by angiotensin II (Ang-II) and hypoxia. The human aortic VECs were divided into different groups to observe the changes in
Changes of enzyme activities in the rat myocardium caused by experimental hypoxia with and without ginkgo biloba extract EGb 761 pretreatment. A cytophotometrical study.
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Using cytophotometry activity changes of succinate dehydrogenase, glycerol-3-phosphate dehydrogenase and myofibrillar adenosine triphosphatase, were measured in the rat myocardium under normal and different experimental conditions. After hypoxia all enzyme activities were significantly decreased in
Ginkgo biloba extract (EGb761) inhibits mitochondria-dependent caspase pathway and prevents apoptosis in hypoxia-reoxygenated cardiomyocytes.
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BACKGROUND
EGb761 is a standard extract from the leaves of Ginkgo biloba (Yinxing) containing ginkgo-flavone glycosides and terpenoid. The flavonoid components of EGb761 scavenge free radicals and protect myocardia from ischemia-reperfusion injury. The present study aims to determine the effects of
Protective effects of Ginkgo biloba extract in rats with hypoxia/reoxygenation-induced intestinal injury.
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BACKGROUND
The purpose of this study is to investigate the protective effects of Ginkgo biloba extract (EGb 761) in rat pups with hypoxia/reoxygenation (H/R)-induced bowel injury.
METHODS
One-day-old Wistar albino rat pups (n = 21) were randomly divided into 3 groups: group 1 (control, untreated and
Effect of an extract of Ginkgo biloba on rat brain energy metabolism in hypoxia.
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The purpose of the present investigation was to determine brain energy metabolism under hypoxic conditions as influenced by an extract of Ginkgo biloba (EGB). Male Sprague-Dawley rats treated with EGB were exposed to hypobaric or hypoxic hypoxia, and at various time points during or after hypoxia
[Effects of notoginseng and ginkgo leaf tablets on cardiac function and serum inflammatory factors in hypoxia deacclimatized rats and its mechanism].
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[Effect of Ginkgo biloba extract (EGb50) on mitochondrial function in SH-SY5Y cells after hypoxia/reoxygenation injury].
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Ischemic cerebrovascular disease and cerebral ischemia/reperfusion injury threaten the health of human being. We studied the protective effect of Ginkgo biloba extract 50 (EGb50) on the mitochondrial function in SH-SY5Y cells after hypoxia/reoxygenation (H/R) injury and explored its mechanisms, so
[Effects of Ginkgo biloba extract 50 on hypoxia induced endothelial dysfunction].
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OBJECTIVE
To preliminarily investigate the influence of hypoxia on human umbilical vein endothelial cells (HUVECs), and the effect of Ginkgo biloba extract 50 (GBE50) on it.
METHODS
Flow cytometry, TUNEL, RT-PCR, Western blot, etc. were applied, to study the effect of hypoxia and GBE50 on
Effects of Ginkgo biloba on exhaled nasal nitric oxide during normobaric hypoxia in humans.
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Ginkgo biloba, an extract of the ginkgo tree, may prevent or lessen symptoms of acute mountain sickness in humans. The mechanism of this effect is poorly understood. One hypothesis is that ginkgo alters nitric oxide (NO) metabolism, possibly by scavenging NO or altering nitric oxide synthase
The influence of hypoxia on the myocardium of experimentally diabetic rats with and without protection by Ginkgo biloba extract. III: Ultrastructural investigations on mitochondria.
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Completing our preceding ultrastructural studies on diabetes and additional acute hypoxia of rat myocardium and the protective effect of Ginkgo extract (EGb) we investigated specific ultrastructural-morphometric parameters of corresponding mitochondria. Aim of the study was to answer the question
Experimental hypoxia of STZ-diabetic rat myocardium and protective effects of Ginkgo biloba extract. II. Ultrastructural investigation of microvascular endothelium.
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Four months after induction of diabetes by intraperitonal injection of 60 mg streptozotocin/kg body weight wistar rats were exposed to an acute respiratoric hypoxia of 20 min duration. One group of the rats received daily Ginkgo biloba extract EGb 761 (100 mg/kg body weight). By means of qualitative
Myocardium-protective effects of Ginkgo biloba extract (EGb 761) in old rats against acute isobaric hypoxia. An electron microscopic morphometric study. I. Protection of cardiomyocytes.
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Ginkgo biloba extract EGb 761 was used in hypoxia experiments with old rats to investigate its ultrastructure-preserving effects on the myocardium. Hypoxia was performed by means of a hypoxia chamber combined with a commercial narcosis apparatus. N2O/O2-mixture was applied with O2 at 5 vol.% for 20
Myocardium-protective effects of Ginkgo biloba extract (EGb 761) in old rats against acute isobaric hypoxia. An electron microscopic morphometric study. II. Protection of microvascular endothelium.
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Aim of this electron microscopic morphometric study was to demonstrate ultrastructure protective properties of Ginkgo biloba extract EGb 761 on myocardial microvessels of old rats during acute hypoxic stress. Hypoxia of 20 minutes duration with N2O/O2 mixture (5 vol% O2) was performed using a
Ultrastructural, immunohistochemical and biochemical investigations of the rat liver exposed to experimental diabetes und acute hypoxia with and without application of Ginkgo extract.
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The aim of this paper was to investigate the effect of streptozotocin-induced diabetes by i.p. bolus injection of streptozotocin at 60 mg per kg bodyweight over four months and additional acute respiratory hypoxia (20 min. duration, 5% oxygen v/v), and also the protective effect of Ginkgo biloba
Actions of Ginkgo Biloba related to potential utility for the treatment of conditions involving cerebral hypoxia.
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Neuronal hypoxia results from a variety of cerebrovascular accidents or 'normal' age-associated anatomic changes. The consequences vary from mild deficits in neurologic function to massive neuropathology. Present pharmacotherapeutic therapy is not ideal. Two apparently disparate approaches to the
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