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dihydrocapsaicin/исхемија
Веза се чува у привремену меморију
7 резултати
Dihydrocapsaicin-induced angiogenesis and improved functional recovery after cerebral ischemia and reperfusion in a rat model.
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This study investigated the long-term effects of dihydrocapsaicin (DHC)-induced angiogenesis and improved functional outcomes in cerebral ischemia and reperfusion (I/R) rats. Middle cerebral artery occlusion was induced in I/R rats for 2 h, followed by reperfusion. The animals were divided into
Dihydrocapsaicin Attenuates Blood Brain Barrier and Cerebral Damage in Focal Cerebral Ischemia/Reperfusion via Oxidative Stress and Inflammatory.
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This study investigated the effect of dihydrocapsaicin (DHC) on cerebral and blood brain barrier (BBB) damage in cerebral ischemia and reperfusion (I/R) models. The models were induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. The rats were divided into five groups:
Dihydrocapsaicin-induced hypothermia after asphyxiai cardiac arrest in rats.
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Cardiac arrest (CA) is one of the leading causes of mortality and morbidity in the world. Fast, reversible and controllable pharmaceutical-induced hypothermia (PIH) is strongly desired to treat ischemia-reperfusion brain injury. Dihydrocapsaicin (DHC), an agonist of transient receptor potential
Dihydrocapsaicin (DHC) enhances the hypothermia-induced neuroprotection following ischemic stroke via PI3K/Akt regulation in rat.
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OBJECTIVE
Hypothermia has demonstrated neuroprotection following ischemia in preclinical studies while its clinical application is still very limited. The aim of this study was to explore whether combining local hypothermia in ischemic territory achieved by intra-arterial cold infusions (IACIs) with
Transient receptor potential melastatin 8 channel inhibition potentiates the hypothermic response to transient receptor potential vanilloid 1 activation in the conscious mouse.
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OBJECTIVE
Mild decrease in core temperature (therapeutic hypothermia) provides lasting neuroprotection following cardiac arrest or cerebral ischemia. However, current methods for producing therapeutic hypothermia trigger a cold-defense response that must be countered by sedatives, muscle paralytics,
Pharmacologically induced hypothermia via TRPV1 channel agonism provides neuroprotection following ischemic stroke when initiated 90 min after reperfusion.
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Traditional methods of therapeutic hypothermia show promise for neuroprotection against cerebral ischemia-reperfusion (I/R), however, with limitations. We examined effectiveness and specificity of pharmacological hypothermia (PH) by transient receptor potential vanilloid 1 (TRPV1) channel agonism in
Shivering and tachycardic responses to external cooling in mice are substantially suppressed by TRPV1 activation but not by TRPM8 inhibition.
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Mild decrease of core temperature (32-34°C), also known as therapeutic hypothermia, is a highly effective strategy of neuroprotection from ischemia and holds significant promise in the treatment of stroke. However, induction of hypothermia in conscious stroke patients is complicated by
Најкомплетнија база лековитог биља подржана науком
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- Препознавање биљака по слици
- Интерактивна ГПС мапа - означите биље на локацији (ускоро)
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