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geniposide/инфаркт
Веза се чува у привремену меморију
5 резултати
Geniposide reduces inflammatory responses of oxygen-glucose deprived rat microglial cells via inhibition of the TLR4 signaling pathway.
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Geniposide, an iridoid glycoside isolated from Gardenia, has neuroprotective activities against oxidative stress and inflammation. The present study investigated the in vivo protective effect of geniposide on ischemia/reperfusion-injured rats by middle cerebral artery occlusion (MCAO), and the
Inhibition of autophagy by geniposide protects against myocardial ischemia/reperfusion injury
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Geniposide (GP), extracted from a traditional Chinese herb Gardenia jasminoides, has extensive pharmacological effects. But the effects and the potential mechanisms of GP on myocardial ischemia/reperfusion (I/R) injury are poorly understood. In present study, we investigated the effect of GP on
Protective effects of geniposide and ginsenoside Rg1 combination treatment on rats following cerebral ischemia are mediated via microglial microRNA‑155‑5p inhibition.
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Geniposide, an active component of Gardenia, has been reported to protect against cerebral ischemia in animals. Ginsenoside Rg1, a component of Panax notoginseng, is usually administered in combination with Gardenia for the treatment of acute ischemic stroke; however, there are unknown effects of
Geniposide Attenuates Post-Ischaemic Neurovascular Damage via GluN2A/AKT/ ERK-Dependent Mechanism.
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OBJECTIVE
Calcium-permeable ionotropic NMDAR-mediated hyperactivity is regarded as the critical factor in modulating the development of ischaemic stroke. Recently, there has been increasing interest in preventing post-stroke neuronal death by focusing on intervening in the function of subpopulations
Geniposide alleviates hypoxia-induced injury by down-regulation of lncRNA THRIL in rat cardiomyocytes derived H9c2 cells.
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Geniposide (GEN) is an iridoid glycoside extracts from Gardenia jasminoides Ellis with antioxidant and anti-inflammarory properties. The objective of this study was to explore the effects of GEN on a cell model of myocardial infarction (MI). After transfection, hypoxia-stimulated H9c2 cells were
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