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ginkgolide b/infiammazione
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Pagina 1 a partire dal 67 risultati
Ginkgolide B reduces inflammatory protein expression in oxidized low-density lipoprotein-stimulated human vascular endothelial cells.
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Ginkgolide B is a herbal constituent extracted from leaves of the ginkgo biloba tree. Previous studies have shown that ginkgolide B is a specific platelet activating factor (PAF) receptor antagonist, and it suppresses PAF-mediated platelet activation via competitive binding. In this study, the
Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades.
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The current study was undertaken to delineate the protective effect of Ginkgolide B, a phyto-constituent from Ginkgo biloba, on oxidized (ox)-LDL-induced endothelial dysfunction via targeting Lectin-like ox-LDL-receptor-1 (LOX-1), NADPH oxidase 4 (NOX-4), and other inflammatory proteins. Our results
[Inhibitory effect of ginkgolide B on angiogenesis in chronic inflammation].
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OBJECTIVE
To investigate the inhibitory effect of ginkgolide B on angiogenesis in chronic inflammation and the possible mechanisms.
METHODS
The murine chronic granulomatous air pouch model was used to observe the anti-angiogenesis effect of ginkgolide B. The vascular index was determined by
[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
Ginkgolide B reduces atherogenesis and vascular inflammation in ApoE(-/-) mice.
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OBJECTIVE
To investigate whether ginkgolide B (a platelet-activating factor inhibitor) affects vascular inflammation in atherosclerosis-prone apolipoprotein E-deficient (ApoE(-/-)) mice.
RESULTS
Human platelets were used to evaluate the effects of ginkgolide B on platelet aggregation and signal
Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes.
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BACKGROUND
Osteoarthritis (OA) is one of degenerative and chronic diseases of articular joints. Articular cartilage is an avascular tissue, and its primary cellular component is chondrocytes. The main characteristic of OA is non-classic inflammation and cartilage degeneration. Ginkgolide B (GB) is a
Ginkgolide B Suppresses TLR4-Mediated Inflammatory Response by Inhibiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs.
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OBJECTIVE
Ginkgolide B is a Ginkgo biloba leaf extract that has been identified as a natural platelet-activating factor receptor (PAFR) antagonist. We investigated the effect of ginkgolide B on high glucose-induced TLR4 activation in human umbilical vein endothelial cells (HUVECs).
METHODS
Protein
Ginkgolide B protects human pulmonary alveolar epithelial A549 cells from lipopolysaccharide-induced inflammatory responses by reducing TRIM37-mediated NF-κB activation.
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The treatment options for acute stroke combined with pulmonary infection are limited. Clinically, there are several therapies to promote blood circulation and dissipate blood stasis; these treatment options include ginkgolide B (GB), which has PAF (platelet activating factor) inhibiting effects.
Ginkgolide B Mediated Alleviation of Inflammatory Cascades and Altered Lipid Metabolism in HUVECs via Targeting PCSK-9 Expression and Functionality.
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The potential of oxidized-LDL (Ox-LDL) to elicit inflammatory responses in macrophages leading to the atherosclerosis (AS) progression is well known. Since proprotein convertase subtilisin/Kexin-9 (PCSK-9), the posttranslational regulator of LDL-receptor, is associated with elevated LDL in the
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
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
A novel anti-inflammatory role for ginkgolide B in asthma via inhibition of the ERK/MAPK signaling pathway.
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Ginkgolide B is an anti-inflammatory extract of Ginkgo biloba and has been used therapeutically. It is a known inhibitor of platelet activating factor (PAF), which is important in the pathogenesis of asthma. Here, a non-infectious mouse model of asthma is used to evaluate the anti-inflammatory
Ginkgolide B promotes osteoblast differentiation via activation of canonical Wnt signalling and alleviates osteoporosis through a bone anabolic way.
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Osteoporosis has become a worldwide problem as the population ages. Although many advances have been made in the treatment of osteoporosis in the past few years, the outcome are sometimes disturbing because of the adverse effects of these treatments. Further studies are still needed to identify
Effect of ginkgolide B on the platelet-activating factor induced changes of chemotaxis and cytoskeleton of macrophages.
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OBJECTIVE
To study the inhibitory effect of ginkgolide B (BN52021) on the PAF induced changes of chemotaxis of murine peritoneal macrophages and the related polymerization of F-actin.
METHODS
Chemotaxis assays were performed using a modified 48-well Boyden chamber. Actin polymerization of murine
Platelet activating factor (PAF) antagonism with ginkgolide B protects the liver against acute injury. importance of controlling the receptor of PAF.
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Platelet activating factor (PAF) is an ubiquitous phospholipid that acts as a mediator of numerous pathophysiological conditions, including hepatotoxicity. The present study has been conducted to evaluate the eventual role of the platelet activating factor in post-acetaminophen intoxication of
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