Aneurysmal Subarachnoid Hemorrhage: an Overview of Inflammation-Induced Cellular Changes

Coulibaly, Aminata P.; Provencio, J. Javier

doi:10.1007/s13311-019-00829-x

Cited by 67 publications

(65 citation statements)

References 71 publications

(122 reference statements)

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“…By contrast, an important feature of SAH is that there is a delayed phase of brain injury at 3-14 days after hemorrhage in about a third of patients (Macdonald and Schweizer, 2017). The neuronal destruction continues from the EBI phase to the delayed injury phase, resulting in the continuous neurological deterioration (Coulibaly and Provencio, 2020). Considering that neurons are hard to regenerate, this persistent neuronal irreversible structural damage and loss of neurological functions worsen the SAH patients' poor neurological functional outcomes.…”

Section: Discussionmentioning

confidence: 99%

Bakuchiol Attenuates Oxidative Stress and Neuron Damage by Regulating Trx1/TXNIP and the Phosphorylation of AMPK After Subarachnoid Hemorrhage in Mice

Liu

Guo

et al. 2020

Front. Pharmacol.

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Subarachnoid hemorrhage (SAH) is a fatal cerebrovascular condition with complex pathophysiology that reduces brain perfusion and causes cerebral functional impairments. An increasing number of studies indicate that early brain injury (EBI), which occurs within the first 72 h of SAH, plays a crucial role in the poor prognosis of SAH. Bakuchiol (Bak) has been demonstrated to have multiorgan protective effects owing to its antioxidative and anti-inflammatory properties. The present study was designed to investigate the effects of Bak on EBI after SAH and its underlying mechanisms. In this study, 428 adult male C57BL/6J mice weighing 20 to 25 g were observed to investigate the effects of Bak administration in an SAH animal model. The neurological function and brain edema were assessed. Content of MDA/3-NT/8-OHdG/superoxide anion and the activity of SOD and GSH-Px were tested. The function of the blood-brain barrier (BBB) and the protein levels of claudin-5, occludin, zonula occludens-1, and matrix metalloproteinase-9 were observed. TUNEL staining and Fluoro-Jade C staining were conducted to evaluate the death of neurons. Ultrastructural changes of the neurons were observed under the transmission electron microscope. Finally, the roles of Trx, TXNIP, and AMPK in the protective effect of Bak were investigated. The data showed that Bak administration 1) increased the survival rate and alleviated neurological functional deficits; 2) alleviated BBB disruption and brain edema; 3) attenuated oxidative stress by reducing reactive oxygen species, MDA, 3-NT, 8-OHdG, gp91 phox , and 4-HNE; increased the activities of SOD and GSH-Px; and alleviated the damage to the ultrastructure of mitochondria; 4) inhibited cellular apoptosis by regulating the protein levels of Bcl-2, Bax, and cleaved caspase-3; and 5) upregulated the protein levels of Trx1 as well as the phosphorylation of AMPK and downregulated the protein levels of TXNIP. Moreover, the protective effects of Bak were partially reversed by PX-12 and compound C. To summarize, Bak attenuates EBI after SAH by alleviating BBB disruption, oxidative

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Section: Discussionmentioning

confidence: 99%

Bakuchiol Attenuates Oxidative Stress and Neuron Damage by Regulating Trx1/TXNIP and the Phosphorylation of AMPK After Subarachnoid Hemorrhage in Mice

Liu

Guo

et al. 2020

Front. Pharmacol.

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“…The elevated WBC count after the percutaneous intervention is also reflection of the inflammatory process in the brain tissue, and its association with CVS after SAH was not surprising. It was recently understood that a lot of vascular and neural changes after SAH were caused by inflammation accompanied by the activation of immune cells in brain parenchyma and blood [ 29 ]. There are many autacoids, hormones and neurotransmitters that may cause vasospasm, and some of them are released from platelets, such as serotonin, while the others could originate from other blood cells destroyed after SAH [ 30 , 31 ]; injured neurons also react with increased firing, so local concentrations of vasoactive catecholamines, endothelins or other substances may mount, causing intense and prolonged vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

et al. 2020

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AbstractIntroductionAneurysmal subarachnoid hemorrhage is a type of spontaneous hemorrhagic stroke, which is caused by a ruptured cerebral aneurysm. Cerebral vasospasm (CVS) is the most grievous complication of subarachnoid hemorrhage (SAH). The aim of this study was to examine the risk factors that influence the onset of CVS that develops after endovascular coil embolization of a ruptured aneurysm.Materials and methodsThe study was designed as a cross-sectional study. The patients included in the study were 18 or more years of age, admitted within a period of 24 h of symptom onset, diagnosed and treated at a university medical center in Serbia during a 5-year period.ResultsOur study showed that the maximum recorded international normalized ratio (INR) values in patients who were not receiving anticoagulant therapy and the maximum recorded white blood cells (WBCs) were strongly associated with cerebrovascular spasm, increasing its chances 4.4 and 8.4 times with an increase of each integer of the INR value and 1,000 WBCs, respectively.ConclusionsSAH after the rupture of cerebral aneurysms creates an endocranial inflammatory state whose intensity is probably directly related to the occurrence of vasospasm and its adverse consequences.

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“…The M1 phenotype of microglia is associated with the increase and expansion of cerebral inflammation following SAH, leading to secondary brain injury [ 9 , 10 , 43 , 44 ]. Microglia activation is especially prevalent within the regions in proximity to the hematoma or the SAH inundated basal cisterns and as early as 24 h after the initial rupture.…”

Section: Microglia In the Early Stage Of Sah—the Arrival Of The Stormmentioning

confidence: 99%

“…This then furthers processes of neuronal apoptosis and necrosis, resulting in a subsequent discharge of inflammatory molecules (alarmins) from the nuclei, like high-mobility group box 1 (HMGB1), which in turn sustains the activation of additional microglia [ 45 ]. This self-sustaining process then leads to the recruitment of perivascular macrophages, increased blood–brain barrier permeability, as well as heightened neuronal loss [ 44 , 46 ]. Despite emerging evidence that microglia can be phagocytic, there is no indication that they execute this task in the early stage after SAH.…”

Section: Microglia In the Early Stage Of Sah—the Arrival Of The Stormmentioning

confidence: 99%

Involvement of Microglia in the Pathophysiology of Intracranial Aneurysms and Vascular Malformations—A Short Overview

Florian

Şuşman

2021

IJMS

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Aneurysms and vascular malformations of the brain represent an important source of intracranial hemorrhage and subsequent mortality and morbidity. We are only beginning to discern the involvement of microglia, the resident immune cell of the central nervous system, in these pathologies and their outcomes. Recent evidence suggests that activated proinflammatory microglia are implicated in the expansion of brain injury following subarachnoid hemorrhage (SAH) in both the acute and chronic phases, being also a main actor in vasospasm, considerably the most severe complication of SAH. On the other hand, anti-inflammatory microglia may be involved in the resolution of cerebral injury and hemorrhage. These immune cells have also been observed in high numbers in brain arteriovenous malformations (bAVM) and cerebral cavernomas (CCM), although their roles in these lesions are currently incompletely ascertained. The following review aims to shed a light on the most significant findings related to microglia and their roles in intracranial aneurysms and vascular malformations, as well as possibly establish the course for future research.

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Aneurysmal Subarachnoid Hemorrhage: an Overview of Inflammation-Induced Cellular Changes

Cited by 67 publications

References 71 publications

Bakuchiol Attenuates Oxidative Stress and Neuron Damage by Regulating Trx1/TXNIP and the Phosphorylation of AMPK After Subarachnoid Hemorrhage in Mice

Bakuchiol Attenuates Oxidative Stress and Neuron Damage by Regulating Trx1/TXNIP and the Phosphorylation of AMPK After Subarachnoid Hemorrhage in Mice

Risk factors for cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

Involvement of Microglia in the Pathophysiology of Intracranial Aneurysms and Vascular Malformations—A Short Overview

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