Central Nervous System Tissue Regeneration after Intracerebral Hemorrhage: The Next Frontier

Zhang, Ruiyi; Xue, Mengzhou; Yong, V. Wee

doi:10.3390/cells10102513

Cited by 21 publications

(20 citation statements)

References 242 publications

(262 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After ICH, BBB damage can result from pro-inflammatory cytokines and reactive oxygen species, which are secreted by the excess activation of microglia ( Taylor et al, 2017 ). As well, the MMP-9 produced after ICH can not only enhance inflammation, and perihematomal edema, and cause lesional expansion, but also contribute to BBB disruption by degrading the extracellular matrix ( Zhang et al, 2021 ). Therefore, the NSA-reduced MMP-9 ( Figure 5 ) may help protect the BBB.…”

Section: Discussionmentioning

confidence: 99%

Necrosulfonamide Alleviates Acute Brain Injury of Intracerebral Hemorrhage via Inhibiting Inflammation and Necroptosis

Zhang

Wang

et al. 2022

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

ObjectiveIntracerebral hemorrhage (ICH) is the most lethal subtype of stroke, without effective treatment. Necrosulfonamide (NSA), a specific inhibitor for mixed lineage kinase domain-like protein, has been reported to exert neuroprotective effects in neurological diseases by ameliorating neuroinflammation and necroptosis. We hypothesized that NSA would alleviate acute brain injury and improve behavioral outcomes after ICH.Materials and MethodsMale adult C57BL/6 mice were assigned randomly into three groups. In vehicle and treatment groups, animals were injected with collagenase VII to induce ICH. The solvent (0.25% DMSO) and NSA (5 mg/kg) were administrated intraperitoneally twice a day, respectively. The sham group was injected with saline and administrated with DMSO. The brain hematoma volume, inflammatory factors, and blood-brain barrier permeability were measured on day 3 after the operation. Fluorescent double immunostaining was performed to evaluate the neuronal death. Neurological functions were assessed.ResultsIn the NSA group, the hematoma size was significantly reduced, inflammatory cells and cytokines were suppressed, and the blood-brain barrier was protected compared to vehicle controls. NSA dramatically reduced the death of neurons and improved the performance of neurological functions after ICH.ConclusionNecrosulfonamide has a neuroprotective role in alleviating acute brain injury in a mouse ICH model, and this is associated with reduced neuroinflammation and necroptosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Necrosulfonamide Alleviates Acute Brain Injury of Intracerebral Hemorrhage via Inhibiting Inflammation and Necroptosis

Zhang

Wang

et al. 2022

Front. Mol. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Following ICH or primary injury, a proinflammatory cascade in the peri-hematoma induces neural cell death. This proinflammatory cascade is composed of infiltrated leucocytes, activated astrocytes, and microglia [ 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ], and is associated with the activity of connexin channels.…”

Section: Connexin and Pannexin Channels In Ichmentioning

confidence: 99%

“…SBI is a major cause of the high mortality and morbidity in ICH patients. Until now, only limited treatment options are available for ICH, therefore novel therapeutic options are needed to be developed [ 7 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Gap Junctions and Hemichannels Composed of Connexins and Pannexins Mediate the Secondary Brain Injury Following Intracerebral Hemorrhage

Zhang

Khan

Liu

et al. 2021

Biology

Self Cite

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a devastating disease with high mortality and morbidity; the mortality rate ranges from 40% at 1 month to 54% at 1 year; only 12%−39% achieve good outcomes and functional independence. ICH affects nearly 2 million patients worldwide annually. In ICH development, the blood leakage from ruptured vessels generates sequelae of secondary brain injury (SBI). This mechanism involves activated astrocytes and microglia, generation of reactive oxygen species (ROS), the release of reactive nitrogen species (RNS), and disrupted blood brain barrier (BBB). In addition, inflammatory cytokines and chemokines, heme compounds, and products of hematoma are accumulated in the extracellular spaces, thereby resulting in the death of brain cells. Recent evidence indicates that connexins regulate microglial activation and their phenotypic transformation. Moreover, communications between neurons and glia via gap junctions have crucial roles in neuroinflammation and cell death. A growing body of evidence suggests that, in addition to gap junctions, hemichannels (composed of connexins and pannexins) play a key role in ICH pathogenesis. However, the precise connection between connexin and pannexin channels and ICH remains to be resolved. This review discusses the pathological roles of gap junctions and hemichannels in SBI following ICH, with the intent of discovering effective therapeutic options of strategies to treat ICH.

show abstract

“…Intracerebral hemorrhage (ICH) is a leading health problem with high mortality and adverse outcomes (1)(2)(3). The poor prognosis is attributed to the primary brain injury caused by the hematoma (4), and secondary brain injury attributed to neuroinflammation, excitatory amino acid, oxidative stress (OS), cytotoxicity of blood, hypermetabolism and spreading depression (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets

et al. 2022

Self Cite

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a highly fatal disease with mortality rate of approximately 50%. Oxidative stress (OS) is a prominent cause of brain injury in ICH. Important sources of reactive oxygen species after hemorrhage are mitochondria dysfunction, degradated products of erythrocytes, excitotoxic glutamate, activated microglia and infiltrated neutrophils. OS harms the central nervous system after ICH mainly through impacting inflammation, killing brain cells and exacerbating damage of the blood brain barrier. This review discusses the sources and the possible molecular mechanisms of OS in producing brain injury in ICH, and anti-OS strategies to ameliorate the devastation of ICH.

show abstract

Central Nervous System Tissue Regeneration after Intracerebral Hemorrhage: The Next Frontier

Cited by 21 publications

References 242 publications

Necrosulfonamide Alleviates Acute Brain Injury of Intracerebral Hemorrhage via Inhibiting Inflammation and Necroptosis

Necrosulfonamide Alleviates Acute Brain Injury of Intracerebral Hemorrhage via Inhibiting Inflammation and Necroptosis

Gap Junctions and Hemichannels Composed of Connexins and Pannexins Mediate the Secondary Brain Injury Following Intracerebral Hemorrhage

Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets

Contact Info

Product

Resources

About