Dynamic changes of inflammatory markers in brain after hemorrhagic stroke in humans: A postmortem study

He, Wei; Zhang, Zhiyi; Hu, Xiaoli; Zhao, Ruibo; Song, Yuejia; Ban, Xiang; Qi, Jiping; Wang, Jian

doi:10.1016/j.brainres.2010.04.033

Cited by 68 publications

(53 citation statements)

References 30 publications

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“…Activated microglia and astrocytes and infiltrating macrophages are major inflammatory cells that contribute to secondary brain damage (e.g., brain oedema) after ICH1025. Our histologic data showed that microglia/macrophage activation peaked in the perilesional region on day 3 and then decreased with time.…”

Section: Discussionmentioning

confidence: 58%

Multimodality MRI assessment of grey and white matter injury and blood-brain barrier disruption after intracerebral haemorrhage in mice

Yang

Wang

et al. 2017

Sci Rep

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In this study, we examined injury progression after intracerebral haemorrhage (ICH) induced by collagenase in mice using a preclinical 11.7 Tesla MRI system. On T2-weighted MRI, lesion and striatal volumes were increased on day 3 and then decreased from days 7 to 28. On day 3, with an increase in striatal water content, vasogenic oedema in the perihaematomal region presented as increased T2 and increased apparent diffusion coefficient (ADC) signal. With a synchronous change in T2 and ADC signals, microglial activation peaked on day 3 in the same region and decreased over time. Iron deposition appeared on day 3 around the haematoma border but did not change synchronously with ADC signals. Vascular permeability measured by Evans blue extravasation on days 1, 3, and 7 correlated with the T1-gadolinium results, both of which peaked on day 3. On diffusion tensor imaging, white matter injury was prominent in the corpus callosum and internal capsule on day 3 and then partially recovered over time. Our results indicate that the evolution of grey/white matter injury and blood-brain barrier disruption after ICH can be assessed with multimodal MRI, and that perihaematomal vasogenic oedema might be attributable to microglial activation, iron deposition, and blood-brain barrier breakdown.

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Section: Discussionmentioning

confidence: 58%

Multimodality MRI assessment of grey and white matter injury and blood-brain barrier disruption after intracerebral haemorrhage in mice

Yang

Wang

et al. 2017

Sci Rep

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“…Wu et al [46] confirmed the upregulation of MMP-9 in spontaneous ICH up to 5 days after hemorrhage onset. Additionally, NF-ĸB, p65 and macrophage inflammatory protein-2 were overexpressed, showing predominance at the hematoma site.…”

Section: Mmps and Human Spontaneous Ichmentioning

confidence: 59%

“…Wu et al [46] investigated the timing of secondary brain damage in patients with spontaneous ICH who underwent hematoma evacuation. Apart from increased levels of MMP-9, they observed overexpression of caspase-3 and proliferation of terminal uridine nick-end labeling-positive cells as early as 6 h after spontaneous ICH onset with the tendency to progression up to 24 h, limited by the duration of the observation.…”

Section: Mmps and Human Spontaneous Ichmentioning

confidence: 99%

Matrix Metalloproteinases in Human Spontaneous Intracerebral Hemorrhage: An Update

et al. 2012

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Background: In default of a plausible and satisfactory causal treatment for hemorrhagic stroke, a role of matrix metalloproteinases (MMPs) in the pathogenesis of cerebrovascular diseases has recently been widely discussed. The well-known impact of MMPs on extracellular matrix destruction triggered by inflammation as a foundation for several diseases, including stroke, is very much in evidence. Newly, some additional aspects of MMP function considering their intracellular activity crucial for neuronal death following ischemic brain damage have emerged. The effect of blood-brain barrier disruption caused by MMPs on the prognosis in patients suffering from spontaneous intracerebral hemorrhage (ICH) has been of interest since it throws a new light upon the pathogenesis, course and possible therapeutic approaches for this least treatable and at the same time most life-threatening form of stroke. Hence, we primarily aimed to review the current clinical knowledge on the significance of metalloproteinase activation in the course of spontaneous intracranial hemorrhage in humans. We also provide a brief characterization of the MMP enzyme family and report on the latest findings on issues arising from experimental studies. Methods: A Medline search using the following key words was performed: matrix metalloproteinases + spontaneous intracerebral hemorrhage/intracranial hemorrhage/bleeding/hemorrhagic stroke. We accepted studies reporting on MMP expression in adult patients with spontaneous ICH, as well as its relation to radiological and clinical features and patients’ outcome. For the final review, 18 clinical studies were considered. MMP inhibition was reviewed on the basis of 11 relevant experimental studies. Also, some relevant reports on the biology of MMPs and their pathophysiology in ICH were reviewed. Results and Conclusions: Many studies provide convincing evidence of a detrimental role of MMPs in ICH, stressing their association with neuroinflammation. The role of MMPs in hemorrhagic stroke appears critical for hematoma and brain edema growth as well as for neuronal death, which are understood as secondary brain injury and may have a considerable clinical impact. Although data on human spontaneous ICH are scarce and mostly based on small populations, they reveal the apparent correlation between MMPs and clinical and radiological ICH features as well as the functional outcome, which might rationalize future therapeutic strategies. However, attempts at MMP inhibition in spontaneous ICH have solely been made under experimental conditions and were associated with a wide range of possible side effects. Therefore, further comprehensive, elucidating investigations in this field are vital before any conclusions could be translated to humans.

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“…It causes perihematomal edema, elevations in intracranial pressure, and neurologic deficits (Keep, et al, 2014). Hematoma formation, expansion, and mass effect cause the primary damage, whereas inflammatory response and oxidative stress contribute to the progression of secondary injury (Wang, 2010, Wu, et al, 2010). Because outcomes are poor, it is worth exploring approaches that can ameliorate the detrimental effects of neuroinflammation and improve functional recovery after ICH.…”

Section: Introductionmentioning

confidence: 99%

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

Jiang

Zuo

Wang

et al. 2016

Neurobiology of Aging

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In this study, we examined the effect of progesterone on histopathologic and functional outcomes of intracerebral hemorrhage (ICH) in 10–12-month-old mice. Progesterone or vehicle was administered by intraperitoneal injection 1 hour after collagenase-induced ICH and then by subcutaneous injections at 6, 24, and 48 hours. Oxidative and nitrosative stress were assayed at 12 hours post-ICH. Injury markers were examined on day 1, and lesion was examined on day 3. Neurologic deficits were examined for 28 days. Progesterone posttreatment reduced lesion volume, brain swelling, edema, and cell degeneration and improved long-term neurologic function. These protective effects were associated with reductions in protein carbonyl formation, protein nitrosylation, and MMP-9 activity and attenuated cellular and molecular inflammatory responses. Progesterone also reduced VEGF expression, increased neuronal-specific Na+/K+ ATPase α3 subunit expression, and reduced PKC-dependent Na+/K+ ATPase phosphorylation. Furthermore, progesterone reduced glial scar thickness, myelin loss, brain atrophy, and residual injury volume on day 28 after ICH. With multiple brain targets, progesterone warrants further investigation for its potential use in ICH therapy.

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Dynamic changes of inflammatory markers in brain after hemorrhagic stroke in humans: A postmortem study

Cited by 68 publications

References 30 publications

Multimodality MRI assessment of grey and white matter injury and blood-brain barrier disruption after intracerebral haemorrhage in mice

Multimodality MRI assessment of grey and white matter injury and blood-brain barrier disruption after intracerebral haemorrhage in mice

Matrix Metalloproteinases in Human Spontaneous Intracerebral Hemorrhage: An Update

Progesterone exerts neuroprotective effects and improves long-term neurologic outcome after intracerebral hemorrhage in middle-aged mice

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