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Sida 1 från 25 resultat
Effects of heme oxygenase 1 on brain edema and neurologic outcome after cardiopulmonary resuscitation in rats.
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BACKGROUND
Heme oxygenase 1 (HO-1) has been shown to attenuate neuronal injury. Therefore, the authors examined whether HO-1 would reduce the brain damage caused by cardiac arrest.
METHODS
Rats anesthetized with halothane were subjected to 8 min of cardiac arrest by asphyxia without any pretreatment
Histopathological and immunohistochemical alterations in rat heart after thyroidectomy and the role of hemin and ketoconazole in treatment.
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The heart is a major target organ for thyroid hormone action and marked changes occur in cardiac function in the case of hypo- or hyperthyroidism. Also, thyroid hormone has a significant regulatory effect on the rate of heme oxidation in the liver. Heme oxygenase (HO) is a heme-catabolizing enzyme
Hemin inhibits cyclooxygenase-2 expression through nuclear factor-kappa B activation and ornithine decarboxylase expression in 12-O-tetradecanoylphorbol-13-acetate-treated mouse skin.
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Inflammation induced by various stimuli has been found to be associated with increased risk for most types of human cancer. Inflammation facilitates the initiation of normal cells, as well as the growth of initiated cells and their progression to malignancy through production of proinflammatory
Hemin Promotes Corneal Allograft Survival Through the Suppression of Macrophage Recruitment and Activation.
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UNASSIGNED
To explore the roles of hemin in preventing corneal allograft rejection (CGR) and the underlying mechanisms.
UNASSIGNED
Hemin (30 mg/kg) was intraperitoneally injected into rats with a corneal allograft on alternate days, from the day of transplantation until euthanasia. The clinical
Hemin Causes Lung Microvascular Endothelial Barrier Dysfunction by Necroptotic Cell Death.
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Hemin, the oxidized prosthetic moiety of hemoglobin, has been implicated in the pathogenesis of acute chest syndrome in patients with sickle cell disease by virtue of its endothelial-activating properties. In this study, we examined whether hemin can cause lung microvascular endothelial barrier
Adipose-derived mesenchymal stem cells stereotactic transplantation alleviate brain edema from intracerebral hemorrhage.
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Adipose-derived mesenchymal stromal cells (ADSCs) exhibited high potential in tissue repair and regeneration, and it has been proved that ADSCs could protect brain cells from apoptosis and maintaining blood-brain barrier stability after cerebral vascular disease. In this study, we evaluated the
Brain edema after experimental intracerebral hemorrhage: role of hemoglobin degradation products.
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OBJECTIVE
The mechanisms involved in brain edema formation following intracerebral hemorrhage (ICH) have not been fully elucidated. The authors have found that red blood cell lysis plays an important role in edema development after ICH. In the present study, they sought to determine whether
Hemin inhibits NLRP3 inflammasome activation in sepsis-induced acute lung injury, involving heme oxygenase-1.
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NLRP3 inflammasome activation contributes to acute lung injury (ALI), accelerating caspase-1 maturation, and resulting in IL-1β and IL-18 over-production. Heme oxygenase-1 (HO-1) plays a protective role in ALI. This study investigated the effect of hemin (a potent HO-1 inducer) on NLRP3 inflammasome
Heme oxygenase-1 modulates thrombomodulin and activated protein C levels to attenuate lung injury in cecal ligation and puncture-induced acute lung injury mice.
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Acute lung injury (ALI) is often associated with sepsis and is the most common cause of acute respiratory failure. The authors evaluated the role of the heme oxygenase (HO)/carbon monoxide (CO) system on lung injury in a cecal ligation and puncture (CLP)-induced mouse model of ALI. The authors
NEMO-binding domain peptides alleviate perihematomal inflammation injury after experimental intracerebral hemorrhage.
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Inflammation aggravates the lethal consequences of intracerebral hemorrhage. Recently, many studies have found that nuclear factor-κB (NF-κB) is a crucial transcription factor that initiates inflammation in the perihematomal region of ICH. NF-κB essential modulator (NEMO)-binding domain (NBD)
Caveolin-1 deletion reduces early brain injury after experimental intracerebral hemorrhage.
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Intracerebral hemorrhage (ICH) is a subtype of stroke with high rates of morbidity and mortality. Caveolin-1 (Cav-1) is the main structural protein of caveolae and is involved in regulating signal transduction and cholesterol trafficking in cells. Although a recent study suggests a protective role
The heme oxygenase system attenuates pancreatic lesions and improves insulin sensitivity and glucose metabolism in deoxycorticosterone acetate hypertension.
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Recent clinical reports indicate that impaired glucose tolerance is a common phenomenon in primary aldosteronism. Aldosterone stimulates NF-kappaB and activating protein-1 (AP-1) to cause oxidative injury. Elevated oxidative stress impairs insulin signaling. We recently showed that the heme
Levetiracetam, an antiepileptic drug has neuroprotective effects on intracranial hemorrhage injury.
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Intracranial hemorrhage (ICH) is a devastating disease that induces hematoma formation with poor neuronal outcome. Levetiracetam (LEV) has been approval for epilepsy seizures. In a previous study, LEV exerted protective effects on cerebral ischemia models; however, the detail effects and the
Effects of heme oxygenase-1 inducers on established rat adjuvant arthritis.
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Heme oxygenase-1 (HO-1) activity can inhibit inflammatory and immune responses. We have examined the influence of HO-1 induction on the established rat adjuvant arthritis model of chronic inflammation. Therapeutic administration of cobalt protoporphyrin IX (CoPP; 5 mg/kg/day i.p.) from day 17 to 23
A novel Nrf2 activator, RS9, attenuates secondary brain injury after intracerebral hemorrhage in sub-acute phase.
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The poor prognosis of intracranial hemorrhage (ICH) is attributed to secondary brain injury (SBI), which is caused by oxidative stress. Blood components induce reactive oxygen species (ROS) over-production and cause cytotoxicity. We focused on the antioxidant system and investigated nuclear
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