Combination of HBO and Memantine in Focal Cerebral Ischemia: Is There a Synergistic Effect?

Feng, Wenfang; Liang, Wei; Lei, Chong; Kinden, Renée; Sang, Hanfei; Xie, Yaning; Huang, Yi; Qu, Yan; Xiong, Lize

doi:10.1007/s12035-014-8949-5

Cited by 20 publications

(21 citation statements)

References 39 publications

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“…Our study showed that concentration of thiol groups in plasma proteins in poststroke patients is approximately 20% lower than in the control group of healthy subjects ( Figure 2 ). Analogous results are obtained by Tsai et al and Wang et al who studied the relationship between oxidative stress and the occurrence of other side effects in patients with acute stroke [ 64 , 65 ]. Moreover, Tsai et al postulated that the level of free thiol groups was significantly lower in patients with large-vessel disease than in those with small-vessel disease in the acute phase of stroke [ 64 ].…”

Section: Discussionsupporting

confidence: 80%

Poststroke Depression as a Factor Adversely Affecting the Level of Oxidative Damage to Plasma Proteins during a Brain Stroke

Cichoń

Bijak

Miller

et al. 2015

Oxidative Medicine and Cellular Longevity

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Poststroke depression, the second most serious psychosomatic complication after brain stroke, leads to delay of the rehabilitation process and is associated with an increased disability and cognitive impairment along with increase in term mortality. Research into the biochemical changes in depression is still insufficiently described. The aim of our study was therefore to evaluate the possible association between plasma protein oxidative/nitrative damages and the development of poststroke depression. We evaluated oxidative/nitrative modifications of specific proteins by measurement of 3-nitrotyrosine and carbonyl groups levels using ELISA test. Additionally, we checked differences in proteins thiol groups by spectrophotometric assay based on reaction between DTNB and thiols. We also evaluated catalase activity in erythrocytes measured as ability to decompose H2O2. Correlation analysis was performed using Spearman's rank. We observed significant (P < 0.001) differences in all oxidative/nitrative stress parameters in brain stroke patients compared to healthy group. Our research shows that oxidative damage of proteins is correlated with the degree of poststroke depression, while nitrative changes do not show any relationship. We demonstrate a positive correlation between the concentration of carbonyl groups and the Geriatric Depression Scale and a negative correlation between the degree of depression and the concentration of -SH groups or catalase activity.

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Section: Discussionsupporting

confidence: 80%

Poststroke Depression as a Factor Adversely Affecting the Level of Oxidative Damage to Plasma Proteins during a Brain Stroke

Cichoń

Bijak

Miller

et al. 2015

Oxidative Medicine and Cellular Longevity

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“…A rat model of MCAO was generated as described previously [35,36]. Briefly, individual rats were anesthetized intraperitoneally with Zoletil (50 mg/kg, Virbac).…”

Section: A Rat Model Of Middle Cerebral Artery Occlusion Treatmentmentioning

confidence: 99%

2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-Glucoside Attenuates Ischemia/Reperfusion-Induced Brain Injury in Rats by Promoting Angiogenesis

Zhou

et al. 2016

Planta Med

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Cerebral ischemia can cause brain infarcts, which are difficult to recover due to poor angiogenesis. 2,3,5,4'-Tetrahydroxystilbene-2-O--D-glucoside is a natural polyphenol, has antioxidant and anti-inflammatory activity, and can protect from ischemic neuronal injury. However, little is known about the effect of 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside on brain microcirculation after stroke. This study aimed at investigating the influence of 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside on brain lesions and angiogenesis after stroke. Sprague-Dawley rats were subjected to right middle cerebral artery occlusion and treated with vehicle, nimodipine, or different doses of 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside daily beginning at 6 h post-middle cerebral artery occlusion for 14 days. The volume of cerebral infarcts, degree of neurological dysfunction, and level of microvessel density were determined longitudinally. The levels of vascular endothelial growth factor, angiopoietin 1, and angiopoietin receptor-2 expression in the brain lesions were characterized by immunohistochemistry and Western blot assays at 14 days post-middle cerebral artery occlusion. We found that 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside significantly promoted postoperative recovery in rats by minimizing the volume of cerebral infarcts and improving neurological dysfunction in a dose- and time-dependent manner. Additionally, 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside significantly increased the microvessel density in the brain and upregulated CD31 expression in ischemic penumbra, relative to that in the control. Finally, treatment with 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside significantly upregulated the relative levels of vascular endothelial growth factor, angiopoietin 1, and angiopoietin receptor-2 expression in the brain lesions of rats. Therefore, these data indicated that 2,3,5,4'-tetrahydroxystilbene-2-O--D-glucoside treatment promoted angiogenesis and recovery from ischemia/reperfusion-induced brain injury in rats.

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“…Total infarct volume was calculated by a blinded investigator using an image analysis system (Adobe Photoshop 9.0, Adobe Systems Incorporated, San Jose, CA, USA). Edema correction of infarct volume was calculated using the following equation [ 61 ]: Vedi=Vinfarct× (1−(Vipsi−Vcontra)/Vcontra); Vedi, volume edema corrected infarct; Vinfarct, volume infarct; Vipsi, volume ipsilateral hemisphere; Vcontra, volume contralateral hemisphere.…”

Section: Methodsmentioning

confidence: 99%

Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes

Liu

et al. 2017

Oncotarget

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Ischemic stroke is a cerebrovascular thrombotic disease with high morbidity and mortality. Qi deficiency blood stasis (QDBS) and Yin deficiency blood stasis (YDBS) are the two major subtypes of ischemic stroke according to the theories of traditional Chinese medicine. This study was conducted to distinguish these two syndromes at transcriptomics level and explore the underlying mechanisms. Male rats were randomly divided into three groups: sham group, QDBS/MCAO group and YDBS/MCAO group. Morphological changes were assessed after 24 h of reperfusion. Microarray analysis with circulating mRNA was then performed to identify differential gene expression profile, gene ontology and pathway enrichment analyses were carried out to predict the gene function, gene co-expression and pathway networks were constructed to identify the hub biomarkers, which were further validated by western blotting and Tunel staining analysis. Three subsets of dysregulated genes were acquired, including 445 QDBS-specific genes, 490 YDBS-specific genes and 1676 blood stasis common genes. Our work reveals for the first time that T cell receptor, MAPK and apoptosis pathway were identified as the hub pathways based on the pathway networks, while Nfκb1, Egfr and Casp3 were recognized as the hub genes by co-expression networks. This research helps contribute to a clearer understanding of the pathological characteristics of ischemic stroke with QDBS and YDBS syndrome, the proposed biomarkers might provide insight into the accurate diagnose and proper treatment for ischemic stroke with blood stasis syndrome.

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Combination of HBO and Memantine in Focal Cerebral Ischemia: Is There a Synergistic Effect?

Cited by 20 publications

References 39 publications

Poststroke Depression as a Factor Adversely Affecting the Level of Oxidative Damage to Plasma Proteins during a Brain Stroke

Poststroke Depression as a Factor Adversely Affecting the Level of Oxidative Damage to Plasma Proteins during a Brain Stroke

2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-Glucoside Attenuates Ischemia/Reperfusion-Induced Brain Injury in Rats by Promoting Angiogenesis

Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes

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