A rat model of chronic subdural hematoma: Insight into mechanisms of revascularization and inflammation

Quan, Wei; Zhang, Zhifei; Tian, Qilong; Wen, Xiaolong; Yu, Peng; Wang, Dong; Cui, Weiyun; Zhou, Lei; Park, Eugene; Baker, Andrew J.; Zhang, Jianning; Jiang, Rongcai

doi:10.1016/j.brainres.2015.08.017

Cited by 34 publications

(30 citation statements)

References 49 publications

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“…The lack of a full parallelism between the increases of vascular number and area might be related to the transient expression of CD43 in endothelial cells during angiogenesis, which could limit the increase of the sum area of the new microvasculature. The elevation of VEGF and Ang-2 levels in the ICH relative to Sham groups is consistent with a lesion response [61][62][63][64][65][66][67]. Importantly, the levels of these two angiogenic factors were significantly higher in the drug-treated than the vehicle-treated groups at most surviving time points (i.e., VEGF in the ICH vs. ICH + NBP25 groups at 7d and 15d, and Ang-2 in the ICH vs. the ICH + NBP10 and ICH vs. ICH + NBP25 groups at all surviving time points).…”

Section: Discussionsupporting

confidence: 65%

“…In healthy adult brain, VEGF is expressed at low levels and is only sporadically detectable in most brain regions [61]. Following ischemic or hypoxic insults, VEGF expression in the brain or the periphery is upregulated to stimulate endothelial cell proliferation and formation of new blood vessels [62][63][64]. Ang-2 is another important soluble factor for angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Ang-2 can facilitate the response of vascular endothelial cells to VEGF [67]. The synergistic effect of these two factors provides a strong support to neovascularization following various central and peripheral injuries or vascular blockage [61][62][63][64][65]. In addition, both factors can play a pathogenic role in the malignant growth of tumors that depends on blood supply via angiogenesis [66][67][68][69].…”

Section: Discussionmentioning

confidence: 99%

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Dl-3-n-Butylphthalide promotes neovascularization and neurological recovery in a rat model of intracerebral hemorrhage

Chen

Tan

et al. 2020

BMC Neurosci

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Background: Cerebral stroke occurs following ischemic and hemorrhagic lesions in the brain. Survival and recovery of stroke patients depend on the severity of the initial injury but also the therapeutic approaches applied for emergent lifesaving and continuing post-stroke management. Dl-3-n-Butylphthalide (NBP), an active compound derived from Chinese celery seeds, has shown clinical efficacy in the treatment of ischemic cerebral stroke. Results: In the present study we explored the therapeutic effect of NBP in a rat model of intracerebral hemorrhage (ICH), focusing on its potential role in promoting neovascularization in the perihemorrhagic zone. ICH was induced in male Sprague-Dawley rats by unilateral injection of autologous blood into the globus pallidus, with sham-operated (Sham group), vehicle-treated (ICH) and NBP-treated (at 10 and 25 mg/kg/Bid, p.o., ICH + NBP10 and ICH + NBP25, respectively) groups examined behaviorally, macroscopically, histologically and biochemically at 1, 3, 7 and 15 days (d) post operation. Rats in the ICH + NBP10 and ICH + NBP25 groups showed reduced Longa's motor scores relative to the ICH groups at the 3 and 7d time points, while the hematoma volume was comparable in the two NBP relative to the ICH groups as measured at 7d and 15d. In the perihemorrhagic zone, the numeric density of blood vessels immunolabeled by CD34, an angiogenic marker, was greater in the ICH + NBP10 and ICH + NBP25 than ICH groups, more so in the higher dosage group, at 1, 3, 7 and 15d. Levels of the vascular endothelial growth factor (VEGF) and angiopoietins-2 (Ang-2) proteins were elevated in the NBP groups relative to the sham and vehicle controls in immunoblotting of tissue lysates from the injection region. Conclusion: These results suggest that NBP can alleviate neurological defects following experimentally induced local brain hemorrhage, which is associated with a potential role of this drug in promoting neovascularization surrounding the bleeding loci.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dl-3-n-Butylphthalide promotes neovascularization and neurological recovery in a rat model of intracerebral hemorrhage

Chen

Tan

et al. 2020

BMC Neurosci

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“…Male, 6 months old Wistar rats (Institute of Bioengineering, Chinese Academy of Sciences) were subject to CSDH model following previously published procedures with minor modifications noted below [21]. Briefly, rats were anesthetized with 10% chloride hydrate solution (3.0 ml/kg, administered via intraperitoneal injection) and positioned in a stereotaxic frame (Stoelting, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Magnetic resonance imaging (MRI) using a 3.0 T instrument (MAGNETOM Spectra 3.0T, Germany) was employed to verify successful CSDH formation and measure the hematoma volume on days 3, 14, and 21 after first blood infusion. The specific coil (HD 8Ch High Brain Array, GE) was used, and the volume of the CSDH was measured based on the GE MRI T2WI scan with 1mm cuts, based on previous publications [21]. Intracranial hematoma volume was calculated based on T2WI images and by histopathology.…”

Section: Methodsmentioning

confidence: 99%

Role of Regulatory T cells in Atorvastatin Induced Absorption of Chronic Subdural Hematoma in Rats

Quan

Zhang

et al. 2019

Aging and disease

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Chronic subdural hematoma (CSDH) is a neurological disorder with a substantial recurrence rate. Atorvastatin is an effective drug for treating hyperlipidemia and known to improve neurological outcome after intracerebral hemorrhage. Previous studies have reported that atorvastatin treatment promotes hematoma absorption in CSDH, while the underlying mechanisms remain unclear. In this study, we investigated whether the anti-inflammatory effects of atorvastatin mediate absorption of CSDH. 144 male, Wistar rats (6 months old) were randomly divided into the following groups: 1) sham surgery control, 2) treatment: CSDH + atorvastatin, and 3) vehicle control: CSDH + saline. Atorvastatin or saline was orally administered daily for 19 days after CSDH procedure. A T2WI MRI was used to evaluate CSDH volume changes during the time course of the study. Flow cytometry and immunohistochemical staining were used to measure the number of regulatory T cells (Treg). ELISA was used to measure cytokine level in the hematoma border. Neurological function and cognitive outcome were evaluated using Foot-Fault test and Morris Water Maze test, respectively. When compared to saline treatment, atorvastatin treatment accelerated the absorption of CSDH as indicated by decreased hematoma volume in T2WI MRI data on 14th and 21st day after CSDH (P<0.05). Atorvastatin treatment significantly increased the number of Treg in circulation and hematoma border from 3rd to 21st day after CSDH. Atorvastatin treatment significantly decreased the levels of interleukins (IL-6 and IL-8) and tumor necrosis factor-α (TNF-α), but increased IL-10 level in the hematoma border. Atorvastatin treatment also improved neurological function and cognitive outcome compared to vehicle treated group. Atorvastatin induced anti-inflammatory responses and increased Treg in circulation and brain which may contribute to the accelerated CSDH absorption in rats.

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Experimental Models of Chronic Subdural Hematoma

2021

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A rat model of chronic subdural hematoma: Insight into mechanisms of revascularization and inflammation

Cited by 34 publications

References 49 publications

Dl-3-n-Butylphthalide promotes neovascularization and neurological recovery in a rat model of intracerebral hemorrhage

Dl-3-n-Butylphthalide promotes neovascularization and neurological recovery in a rat model of intracerebral hemorrhage

Role of Regulatory T cells in Atorvastatin Induced Absorption of Chronic Subdural Hematoma in Rats

Experimental Models of Chronic Subdural Hematoma

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