scholarly journals Rosuvastatin Nanomicelles Target Neuroinflammation and Improve Neurological Deficit in a Mouse Model of Intracerebral Hemorrhage

2021 ◽  
Vol Volume 16 ◽  
pp. 2933-2947
Author(s):  
Liu Zi ◽  
Wencheng Zhou ◽  
Jiake Xu ◽  
Junshu Li ◽  
Ning Li ◽  
...  
Keyword(s):  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Neurological Deficit

scholarly journals Heat shock protein 70 upregulation by geldanamycin reduces brain injury in a mouse model of intracerebral hemorrhage

2010 ◽  
Vol 57 (7) ◽  
pp. 844-850 ◽  
Author(s):  
Anatol Manaenko ◽  
Nancy Fathali ◽  
Hank Chen ◽  
Hidenori Suzuki ◽  
Shammah Williams ◽  
...  
Keyword(s):  
Brain Injury ◽  
Heat Shock ◽  
Mouse Model ◽  
Heat Shock Protein ◽  
Intracerebral Hemorrhage ◽  
Heat Shock Protein 70

scholarly journals [125 I]IodoDPA-713 Binding to 18 kDa Translocator Protein (TSPO) in a Mouse Model of Intracerebral Hemorrhage: Implications for Neuroimaging

2018 ◽  
Vol 12 ◽  
Author(s):  
Frederick Bonsack ◽  
Catherine A. Foss ◽  
Ali S. Arbab ◽  
Cargill H. Alleyne ◽  
Martin G. Pomper ◽  
...  
Keyword(s):  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Translocator Protein

scholarly journals Magnetic Resonance Imaging Reveals Significantly Increased Cerebral Blood Flow in the Hemoglobin E Mouse Model

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 2034-2034
Author(s):  
Min-Hui Cui ◽  
Craig A Branch ◽  
Rhoda Elison Hirsch
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Left Ventricular ◽  
Hemoglobin E ◽  
Significant Difference ◽  
Normal Background

Abstract Hemoglobin E (HbE) is the most common hemoglobin mutation world-wide. EE individuals exhibit a mild anemia as do those with β-thalassemia trait. A paradox arises with the combination of two relatively benign genes in HbE/β-thalassemia (HbE/β-thal) giving rise to highly morbid symptoms, anemia, growth retardation, developmental retardation, thalassemic bone type development, chronic leg ulcers (for a review, S Fucharoen and DJ Weatherall 2012) and often early mortality arising from cardiac failure (N Olivieri, Z Pakbaz et al. 2011). One approach to understanding the characteristics of HbE and this paradox was to generate a transgenic mouse model, expressing solely human HbE. This HbE mouse model exhibits a mild oxidative stress that parallels that observed in human EE individuals (QY Chen, EE Bouhassira et al. 2004, QY Chen, ME Fabry et al. 2012). These transgenic mice also exhibit mild cardiac dysfunction with depressed left ventricular contraction. We present here the first evidence of a significant increase in cerebral blood flow in the full knockout HbE (HbEKO) transgenic mouse model expressing solely human HbE compared to both the HbE+HbF (γ, gamma)-globin transgenic mouse, and the normal background C57 mouse. Cerebral blood flow is assessed non-invasively by MRI imaging. All protocols were approved by the Albert Einstein Institutional Animal Care and Use Committee. Comparing the HbEKO mouse (without human γ globin) to the C57 normal background mouse, a significant increase of over 20% in thalamus cerebral blood flow at baseline is observed (p=0.008). There is also an approximate 18% reduction in thalamus cerebral blood flow comparing HbE low γ mice to the full HbEKO (no γ) (p=0.011). Concomitant with these observations, no significant difference is observed comparing these low gamma HbE mice to the normal C57 background mouse (p=0.384). The goodness of the data is also seen in the relatively small variation in cerebral blood flow amongst the individual mice in each subset. These findings are of particular relevance to reports of neurologic symptoms, intracerebral hemorrhage, and brain infarct in HbE/β-thal patients (V Wong, YL Yu et al. 1990, S Das, S Dubey et al. 2019). In conclusion, these results suggest a direct role of HbE RBC initiating altered cerebral blood flow that when further complexed with β-thal could lead to intracerebral hemorrhage and other cerebral pathophysiology. The finding that the HbEKO mice with high HbF are not significantly different in cerebral blood flow from C57 mice may lend further support to therapeutic approaches enhancing the production of HbF in severe hemoglobinopathies, such as in sickle cell anemia, HbE/β-thal, and β-thal individuals. Disclosures No relevant conflicts of interest to declare.

scholarly journals 17β-Estradiol Attenuates Intracerebral Hemorrhage-Induced Blood–Brain Barrier Injury and Oxidative Stress Through SRC3-Mediated PI3K/Akt Signaling Pathway in a Mouse Model

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110384
Author(s):  
Han Xiao ◽  
Jianyang Liu ◽  
Jialin He ◽  
Ziwei Lan ◽  
Mingyang Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Signaling Pathway ◽  
Brain Edema ◽  
Akt Signaling ◽  
Neurological Deficits ◽  
Akt Signaling Pathway ◽  
And Oxidative Stress

Estrogen is neuroprotective in brain injury models, and steroid receptor cofactor 3 (SRC3) mediates estrogen signaling. We aimed to investigate whether and how SRC3 is involved in the neuroprotective effects of 17ß-estradiol (E2) in a mouse model of intracerebral hemorrhage (ICH). Ovariectomized female mice were treated with E2 after autologous blood injection-induced ICH. Brain damage was assessed by neurological deficit score, brain water content, and oxidative stress levels. Blood–brain barrier (BBB) integrity was evaluated by Evan's blue extravasation and claudin-5, ZO-1, and occludin levels. SRC3 expression and PI3K/Akt signaling pathway were examined in ICH mice treated with E2. The effect of SRC3 on E2-mediated neuroprotection was determined by examining neurological outcomes in SRC3-deficient mice undergone ICH and E2 treatment. We found that E2 alleviated ICH-induced brain edema and neurological deficits, protected BBB integrity, and suppressed oxidative stress. E2 enhanced SRC3 expression and PI3K-/Akt signaling pathway. SRC3 deficiency abolished the protective effects of E2 on ICH-induced neurological deficits, brain edema, and BBB integrity. Our results suggest that E2 suppresses ICH-induced brain injury and SRC3 plays a critical role in E2-mediated neuroprotection.

scholarly journals Pertussis Toxin Induced Inflammatory Response Exacerbates Intracerebral Hemorrhage and Ischemic Stroke in Mice

2020 ◽  
Author(s):  
Ming Zou ◽  
Yan Li ◽  
Hui Zhao ◽  
Yan Feng ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Intracerebral Hemorrhage ◽  
Blood Brain Barrier ◽  
Pertussis Toxin ◽  
Brain Inflammation ◽  
Brain Barrier ◽  
Stroke Severity ◽  
Blood Brain

Abstract Background: Stroke is a devastating and debilitating disease and is a leading cause of death worldwide, including intracerebral hemorrhage (ICH) and ischemic stroke. Emerging evidence indicates that inflammatory cascades after hemorrhagic or ischemic stroke makes a great contribution to brain damage, mainly are involved in neuronal cell death, blood-brain-barrier (BBB) destruction and development of vasogenic edema. However, the features and direct effect of brain inflammation following stroke is still unknown. Methods: We adopted the ICH model by injection of collagenase and used a mouse model of transient cerebral ischemia and reperfusion. And pertussis toxin was used to create a pro-inflammatory milieu. Neurodeficits, lesion volume, production of reactive oxygen species (ROS) and inflammatory factors, brain-infiltrating leukocytes and blood-brain-barrier (BBB) destruction were assessed in mice model treated with pertussis toxin or vehicle.Results: Adopting collagenase induced intracerebral hemorrhage mouse model, we show that pertussis toxin-induced systemic inflammation exacerbated neurological deficits, enlarged lesion size and brain perihematomal edema after intracerebral hemorrhage. Pertussis toxin promoted leukocyte infiltration and inflammatory cytokine release in the brain. Moreover, the integrity of the BBB was further disrupted after receiving pertussis toxin in ICH mice. Furthermore, we demonstrated that pertussis toxin increased stroke severity and enhanced brain inflammation in middle cerebral artery occlusion (MCAO) mouse model. Conclusion: Our results suggest that pertussis toxin increases inflammatory response that exacerbates brain injury after intracerebral hemorrhage or ischemic stroke in mouse model.

Adoptive Regulatory T-cell Therapy Attenuates Perihematomal Inflammation in a Mouse Model of Experimental Intracerebral Hemorrhage

2016 ◽  
Vol 37 (5) ◽  
pp. 919-929 ◽  
Author(s):  
Lei-Lei Mao ◽  
Hui Yuan ◽  
Wen-wen Wang ◽  
Yu-jing Wang ◽  
Ming-feng Yang ◽  
...  
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
Cell Therapy ◽  
Intracerebral Hemorrhage ◽  
Regulatory T Cell ◽  
T Cell Therapy
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