Abstract
Intracerebral hemorrhage (ICH) causes an accumulation of blood in the brain parenchyma that disrupts the normal neurological function of the brain. Despite extensive clinical trials, no medical or surgical therapy has shown to be effective in managing ICH, resulting in a poor prognosis for the patients. Urocortin (UCN) is a 40-amino-acid endogenous neuropeptide that belongs to the corticotropin-releasing hormone (CRH) family. The effect of UCN is activated by binding to two G-protein coupled receptors, CRH-R1 and CRH-R2, which are expressed in brain neurons and glial cells in various brain regions. Current research has shown that UCN exerts neuroprotective effects in ICH models via anti-inflammatory effects, which generally reduced brain edema and reduced blood-brain barrier disruption. These effects gradually help in the improvement of the neurological outcome, and thus, UCN may be a potential therapeutic target in the treatment of ICH. This review summarizes the data published to date on the role of UCN in ICH and the possible protective mechanisms underlined.
Highlights
Intracranial hemorrhage is defined as bleeding in the brain parenchyma of the intracranial vault and meningeal spaces [1]
The main objective of this article is to summarize the studies regarding the role of UCN with a focus on physiological and pathological conditions of Intracerebral hemorrhage (ICH), which may potentiate a new strategy for clinical applications
Since no medical or surgical therapy has shown to be effective in managing ICH, neutrophil-to-lymphocyte ratio (NLR) has been reported as a reliable measure of individual inflammatory status and predictor of clinical outcome [38]
Summary
Intracranial hemorrhage is defined as bleeding in the brain parenchyma of the intracranial vault and meningeal spaces [1]. Among Asians, the Han Chinese population has a higher incidence of ICH due to alcohol intake and hypertension [4]. UCN was found in the central nervous system and peripheral tissues [6]. The physiological function of UCN is mediated by CRH receptor 1 (CRH-R1) at the central nervous system and CRH-R2 at peripheral tissues [7]. UCN has been reported to possess various effects such as its ability to activate cellular metabolic pathways that control the functional central nervous system and the other system such as cardiovascular, gastrointestinal, reproductive and immune systems [8,9,10]. Intracerebroventricular treatment with UCN alleviated brain injury region, reduced edema of the brain, and improved blood-brain barrier (BBB) permeability, which generally improved neurological function in ICH animal study. UCN decreases pathological changes in brain injury and neurological deficits in ICH rats
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