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Stranica 1 iz 86 rezultatima
Comparison of the Effects and Mechanism of the Curcumin with Different Drugs in Experimental Vasospasm After Subarachnoid Hemorrhage.
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OBJECTIVE
Cerebral vasospasm following subarachnoid hemorrhage (SAH) is the most important complication that effects the mortality and morbidity of patients with intracranial aneurysm. Today, the mechanisms of vasospasm are not understood in spite of experimental and clinical researches. The aim of
Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation.
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OBJECTIVE
Subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory
[Curcumin improves learning and memory function through decreasing hippocampal TNF-α and iNOS levels after subarachnoid hemorrhage in rats].
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OBJECTIVE
To investigate the effect of curcumin on learning and memory function of rats with subarachnoid hemorrhage (SAH) and the possible mechanism.
METHODS
A total of 30 male Sprague-Dawley rats were randomly divided into three groups: Sham group, SAH group and curcumin (Cur) therapy group.
Curcumin attenuates vascular inflammation and cerebral vasospasm after subarachnoid hemorrhage in mice.
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Cerebral vasospasm is a major cause of death and disability after subarachnoid hemorrhage (SAH); however, clinical therapies to limit the development of cerebral vasospasm are lacking. Although the causative factors underlying the development of cerebral vasospasm are poorly understood, oxidative
[Curcumin alleviates early brain injury following subarachnoid hemorrhage in rats by inhibiting JNK/c-Jun signal pathway].
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Objective To investigate the inhibitory effect of curcumin on early brain injury following subarachnoid hemorrhage (SAH) by inhibiting JNK/ c-Jun signal pathway. Methods Sixty adult male SD rats were randomly divided into four groups: sham operation group (sham group), SAH group, SAH group treated
Differential regulation of cytokines and transcription factors in liver by curcumin following hemorrhage/resuscitation.
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Inflammatory cytokines interleukin 1 (IL-1), IL-2, IL-6, and tumor necrosis factor-alpha (TNF-alpha) have been recognized as important mediators of pathophysiological and immunological events associated with shock. These inflammatory events after hemorrhage and resuscitation are characterized by the
Curcumin inhibits reactive oxygen species formation and vascular hyperpermeability following haemorrhagic shock.
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1. Oxidative stress induced by reactive oxygen species (ROS) is a key mediator of haemorrhagic shock (HS)-induced vascular hyperpermeability. In the present study, curcumin, a natural anti-oxidant obtained from turmeric (Curcuma longa), was tested against HS-induced hyperpermeability and associated
Curcumin Attenuates Hemorrhagic Shock and Blood Replenish Resuscitation-induced Impairment of Pulmonary Barrier Function by Increasing SIRT1 and Reducing Malondialdehyde and TNF-α Contents and Neutrophil Infiltration in Lung in a Dose-Dependent Fashion.
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Uroprotective effects of curcumin in cyclophosphamide-induced haemorrhagic cystitis paradigm.
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The possible uroprotective effects of curcumin have been addressed in the current study. Haemorrhagic cystitis was induced by challenging male Swiss albino rats with a single dose of cyclophosphamide (150 mg/kg, i.p.). Curcumin (200 mg/kg, i.p.) was administered for 10 consecutive days followed by a
Prolonged hydrocephalus induced by intraventricular hemorrhage in rats is reduced by curcumin therapy.
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Prolonged hydrocephalus is a major cause of severe disability and death of intraventricular hemorrhage (IVH) patients. However, the therapeutic options to minimize the detrimental effects of post-hemorrhagic hydrocephalus are limited. Curcumin has been reported to confer neuroprotective effects in
Enhanced Therapeutic Potential of Nano-Curcumin Against Subarachnoid Hemorrhage-Induced Blood-Brain Barrier Disruption Through Inhibition of Inflammatory Response and Oxidative Stress.
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Curcumin and nano-curcumin both exhibit neuroprotective effects in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH). However, the mechanism that whether curcumin and its nanoparticles affect the blood-brain barrier (BBB) following SAH remains unclear. This study investigated
Curcumin, encapsulated in nano-sized PLGA, down-regulates nuclear factor κB (p65) and subarachnoid hemorrhage induced early brain injury in a rat model.
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BACKGROUND
More and more evidence revealed early brain injury (EBI) may determine the final outcome in aneurismal subarachnoid hemorrhage (SAH) patients. This study is of interest to examine the efficacy of nano-particle curcumin (nanocurcumin), a diarylheptanoid, on a SAH-induced EBI
Curcumin reduces brain-infiltrating T lymphocytes after intracerebral hemorrhage in mice.
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T lymphocytes contribute to inflammation, thereby exacerbating neuronal injury after cerebral ischemia. An increasing amount of evidence indicates that inflammation is a key contributor to intracerebral hemorrhage (ICH)-induced secondary brain injury. Curcumin, a low-molecular-weight curry spice
Curcumin inhibits microglia inflammation and confers neuroprotection in intracerebral hemorrhage.
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Much evidence demonstrates that microglia mediated neuroinflammation is an important contributor to the inflammatory injury in intracerebral hemorrhage (ICH). Therefore, the compounds that can inhibit neuroinflammation are greatly needed. In the current study, we examined whether curcumin, present
Curcumin attenuates brain edema in mice with intracerebral hemorrhage through inhibition of AQP4 and AQP9 expression.
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OBJECTIVE
Aquaporins (AQPs) are the water-channels that play important roles in brain water homeostasis and in cerebral edema induced by brain injury. In this study we investigated the relationship between AQPs and a neuroprotective agent curcumin that was effective in the treatment of brain edema
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