Molecular, Cellular and Clinical Aspects of Intracerebral Hemorrhage: Are the Enemies Within?

Abstract

Hemorrhagic stroke is a disease with high incidence and mortality rates. In addition to the mass lesions that result from hemorrhagic stroke, substances such as the blood-derived products (BDP) (hemoglobin (Hb), heme and iron) induce a potent inflammatory response and exert direct toxic effects on neurons, astrocytes, and microglia. In the present review, we discuss the mechanisms of brain injury secondary to hemorrhagic stroke, focusing on the involvement of BDP as major players of cellular redox imbalance, inflammation, and glutamate excitotoxicity. Potential natural mechanisms of protection against free Hb and heme such as haptoglobin and hemopexin, respectively, are highlighted. We finally discuss the experimental and clinical trials targeting free iron and heme scavenging as well as inflammation, as potential new therapies to minimize the devastating effects of hemorrhagic stroke on brain structure and function.

Cattle encephalon glycoside and ignotin reduced white matter injury and prevented post-hemorrhagic hydrocephalus in a rat model of intracerebral hemorrhage

“…ICH causes primary white matter injury by direct mechanical compression and hematoma expansion, and then it induces secondary injury through the coagulation cascade (especially thrombin)17. Furthermore, secondary injury is also aggravated by the metabolic products of the hematoma, such as iron18, zinc protoporphyrin19, and glutamate excitotoxicity20. The inflammatory response that follows ICH also contributes to the white matter injury21.…”

Comment on “Bilirubin: a novel predictor of hemorrhagic transformation and symptomatic intracranial hemorrhage after mechanical thrombectomy”

“…Their high B levels in HT patients were higher than those of the without HT (WHT) group, suggesting that B is an important marker for both mortality and morbidity in ICT. After ICT occurs, erythrocytes begin to undergo hemolysis within minutes as the body's self-defense mechanism against acute brain damage [2]. Firstly, heme is released from erythrocytes by the hemolysis, then the heme is cleaved by hem oxygenase enzyme and as a result of this degradation, biliverdin, iron, and carbon monoxide occurs.…”

“…Firstly, heme is released from erythrocytes by the hemolysis, then the heme is cleaved by hem oxygenase enzyme and as a result of this degradation, biliverdin, iron, and carbon monoxide occurs. Iron is a highly potent toxic agent for the brain and initiates Fenton reaction and lipid peroxidation [2]. It shows the neurotoxic effect by increasing superoxide and hydroxyl radicals and oxidative stress (OS).…”

Possibilities of clinical neuroimaging assessment scales using for patient severity in the onset of cerebral hemorrhagic supratentorial stroke to predict the outcome of the disease acute period

“…Результати. Значення сумарного бала ≥2 за шкалою Hemphill-ICH та ≥8 по ICH-GS асоційовані з підвищенням ризику летального результату відповідно в 7,1 [2,[8][9][10][11][12][13][14][15][16][17][18],0] (р < 0,01) і 4,4 [2,2-9,3] раза (р < 0,01). Шкала Hemphill-ICH характеризується вищою інформативністю для прогнозування вітального прогнозу виходу гострого періоду МГСІ (AUC = 0,84) порівняно зі шкалою ICH-GS (AUC = 0,78, p < 0,05).…”