scholarly journals Volumetric Analysis of Malignant Middle Cerebral Infarction (MMI): Infarction Volume Before Decompressive Hemicraniectomy for MMI is Associated With Poor Consciousness

2021 ◽  
Vol 4 (1) ◽  
pp. 13-20
Author(s):  
Dong Wook Kim ◽  
Haewon Roh ◽  
Won Ki Yoon ◽  
Taek-Hyun Kwon ◽  
Jong Hyun Kim
Keyword(s):  
Cerebral Infarction ◽  
Volumetric Analysis ◽  
Decompressive Hemicraniectomy ◽  
Infarction Volume

scholarly journals Outcome Following Decompressive Hemicraniectomy for Malignant Cerebral Infarction

Stroke ◽  
2015 ◽  
Vol 46 (9) ◽  
pp. 2695-2698 ◽  
Author(s):  
Stephen Honeybul ◽  
Kwok Ming Ho ◽  
Grant Gillett
Keyword(s):  
Cerebral Infarction ◽  
Decompressive Hemicraniectomy

The administration of complement component C9 augments post-ischemic cerebral infarction volume in neonatal rats

2002 ◽  
Vol 325 (3) ◽  
pp. 175-178 ◽  
Author(s):  
Mitchell D. Imm ◽  
Pamela W. Feldhoff ◽  
Richard C. Feldhoff ◽  
Herbert A. Lassiter
Keyword(s):  
Cerebral Infarction ◽  
Complement Component ◽  
Neonatal Rats ◽  
Infarction Volume

Relationship between Plasma D-Dimer Level and Cerebral Infarction Volume in Patients with Nonvalvular Atrial Fibrillation

2013 ◽  
Vol 35 (1) ◽  
pp. 64-72 ◽  
Author(s):  
Mari Matsumoto ◽  
Manabu Sakaguchi ◽  
Shuhei Okazaki ◽  
Shigetaka Furukado ◽  
Masafumi Tagaya ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cerebral Infarction ◽  
Nonvalvular Atrial Fibrillation ◽  
Infarction Volume ◽  
D Dimer

scholarly journals Network pharmacology and molecular docking reveal the effective substances and active mechanisms of Dalbergia Odoriferain protecting against ischemic stroke

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0255736
Author(s):  
Kedi Liu ◽  
Xingru Tao ◽  
Jing Su ◽  
Fei Li ◽  
Fei Mu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Molecular Docking ◽  
Cerebral Infarction ◽  
Binding Sites ◽  
Network Pharmacology ◽  
Dependent Manner ◽  
Bioactive Components ◽  
Neurological Score ◽  
Infarction Volume

Dalbergia Odorifera (DO) has been widely used for the treatment of cardiovascular and cerebrovascular diseasesinclinical. However, the effective substances and possible mechanisms of DO are still unclear. In this study, network pharmacology and molecular docking were used toelucidate the effective substances and active mechanisms of DO in treating ischemic stroke (IS). 544 DO-related targets from 29 bioactive components and 344 IS-related targets were collected, among them, 71 overlapping common targets were got. Enrichment analysis showed that 12 components were the possible bioactive components in DO, which regulating 9 important signaling pathways in 3 biological processes including ‘oxidative stress’ (KEGG:04151, KEGG:04068, KEGG:04915), ‘inflammatory response’(KEGG:04668, KEGG:04064) and ‘vascular endothelial function regulation’(KEGG:04066, KEGG:04370). Among these, 5 bioactive components with degree≥20 among the 12 potential bioactive components were selected to be docked with the top5 core targets using AutodockVina software. According to the results of molecular docking, the binding sites of core target protein AKT1 and MOL002974, MOL002975, and MOL002914 were 9, 8, and 6, respectively, and they contained 2, 1, and 0 threonine residues, respectively. And some binding sites were consistent, which may be the reason for the similarities and differences between the docking results of the 3 core bioactive components. The results of in vitro experiments showed that OGD/R could inhibit cell survival and AKT phosphorylation which were reversed by the 3 core bioactive components. Among them, MOL002974 (butein) had a slightly better effect. Therefore, the protective effect of MOL002974 (butein) against cerebral ischemia was further evaluated in a rat model of middle cerebral artery occlusion (MCAO) by detecting neurological score, cerebral infarction volume and lactate dehydrogenase (LDH) level. The results indicated that MOL002974 (butein) could significantly improve the neurological score of rats, decrease cerebral infarction volume, and inhibit the level of LDH in the cerebral tissue and serum in a dose-dependent manner. In conclusion, network pharmacology and molecular docking predicate the possible effective substances and mechanisms of DO in treating IS. And the results are verified by the in vitro and in vivo experiments. This research reveals the possible effective substances from DO and its active mechanisms for treating IS and provides a new direction for the secondary development of DO for treating IS.

scholarly journals Extracellular Vesicle-Derived microRNA-410 From Mesenchymal Stem Cells Protects Against Neonatal Hypoxia-Ischemia Brain Damage Through an HDAC1-Dependent EGR2/Bcl2 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Jun Han ◽  
Si Yang ◽  
Xiaosheng Hao ◽  
Bo Zhang ◽  
Hongbo Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cerebral Infarction ◽  
Brain Damage ◽  
Neuronal Apoptosis ◽  
Edema Formation ◽  
Infarction Volume ◽  
Hypoxia Ischemia

Hypoxia-ischemia brain damage (HIBD) is a neurological disorder occring in neonates, which is exacerbated by neuronal apoptosis. Mesenchymal stem cells (MSCs)-derived extracellular vesicles (EVs) have been proposed as a promising strategy for treating or preventing ischemia-related diseases. However, their mechanisms in HIBD remain unclear. Thus, we aimed to address the role of EV-derived microRNA (miR)-410 in HIBD. Neonatal HIBD mouse model was constructed using HI insult, from which neurons were isolated, followed by exposure to oxygen glucose deprivation (OGD). EVs were isolated from human umbilical cord (hUC)-derived MSCs. In silico analyses, dual-luciferase reporter gene and chromatin immunoprecipitation assays were adopted to determine relationships among miR-410, histone deacetylase 1 (HDAC1), early growth response protein 2 (EGR2), and B cell lymphoma/leukemia 2 (Bcl2). The functional roles of EV-derived miR-410 were determined using loss- and gain-of functions experiments, and by evaluating neuronal viability, cell-cycle distribution and neuronal apoptosis in vitro as well as modified neurological severity score (mNSS), edema formation, and cerebral infarction volume in vivo. hUC-MSCs-derived EVs protected against HIBD in vivo and inhibited the OGD-induced neuronal apoptosis in vitro. miR-410 was successfully delivered to neurons by hUC-MSCs-EVs and negatively targeted HDAC1, which inversely mediated the expression of EGR2/Bcl2. Upregulation of EV-derived miR-410 promoted the viability but inhibited apoptosis of neurons, which was reversed by HDAC1 overexpression. EV-derived miR-410 elevation reduced mNSS, edema formation, and cerebral infarction volume by increasing EGR2/Bcl2 expression through downregulating HDAC1 expression in vivo. In summary, EV-derived miR-410 impeded neuronal apoptosis by elevating the expression of EGR2/Bcl2 via HDAC1 downregulation, thereby providing a potential strategy for treating or preventing HIBD.

Combination of Isoflurane and Caspase Inhibition Reduces Cerebral Injury in Rats Subjected to Focal Cerebral Ischemia

2004 ◽  
Vol 101 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Satoki Inoue ◽  
John C. Drummond ◽  
Daniel P. Davis ◽  
Daniel J. Cole ◽  
Piyush M. Patel
Keyword(s):  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Neuronal Death ◽  
Recovery Period ◽  
Cerebral Injury ◽  
Delayed Neuronal Death ◽  
Vehicle Group ◽  
Caspase Inhibitor ◽  
Infarction Volume

Background Recent data indicate that the neuroprotective efficacy of isoflurane is not sustained. Delayed neuronal death, mediated in part by apoptosis, contributes to the gradual increase in the size of the infarction. These data suggest that isoflurane may not be able to inhibit delayed neuronal death. The prevention of apoptosis by a caspase inhibitor might provide neuroprotection in addition to that provided by isoflurane. The current study was conducted to determine whether isoflurane-mediated neuroprotection can be made more durable with the administration of z-VAD-fmk, a nonspecific caspase inhibitor. Methods Fasted Wister rats were allocated to awake-zVAD, awake-vehicle, isoflurane-zVAD, or isoflurane-vehicle groups (n = 16/group). Animals were subjected to focal ischemia for 60 min by filament occlusion of the middle cerebral artery. In the awake groups, isoflurane was discontinued after occlusion of the middle cerebral artery. In the isoflurane groups, isoflurane anesthesia was maintained at 1.5 minimum alveolar concentration during occlusion of the middle cerebral artery. Before and after ischemia, daily injections of z-VAD-fmk or vehicle were administered into the lateral cerebral ventricle for 14 days. Neurologic assessment was performed 14 days after ischemia. The volume of cerebral infarction and the number of intact neurons in the periinfarct cortex were determined by image analysis of hematoxylin and eosin-stained coronal brain sections. Results Infarction volume was less in the isoflurane-zVAD group (23 +/- 11 mm, mean +/- SD) than in isoflurane-vehicle, awake-vehicle, and awake-zVAD groups (82 +/- 31, 86 +/- 31, and 59 +/- 25 mm, respectively; P < 0.05). In comparison with the awake-vehicle and isoflurane-vehicle groups, the administration of z-VAD-fmk significantly decreased infarction volume (P < 0.05). The infarction volume between the awake-vehicle and isoflurane-vehicle groups was not different. The number of intact neurons within the periinfarct cortex was significantly less in the awake-vehicle group than in the other three groups (P < 0.05). The isoflurane-zVAD group demonstrated better neurologic function than the awake-vehicle group (P < 0.05). Conclusion These findings are consistent with the premise that ongoing delayed neuronal death, in part mediated by apoptosis, contributes to the progression of cerebral infarction during the recovery period, and its inhibition can provide sustained neuroprotection.

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