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hemin/éidéime

Sábháiltear an nasc chuig an gearrthaisce
AiltTrialacha cliniciúlaPaitinní
Leathanach 1 ó 25 torthaí

Effects of heme oxygenase 1 on brain edema and neurologic outcome after cardiopulmonary resuscitation in rats.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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.

Ní féidir ach le húsáideoirí cláraithe ailt a aistriú
Logáil Isteach / Cláraigh
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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