Enantiomers of 3-pentylbenzo[c]thiophen-1(3H)-one: preparation and evaluation of anti-ischemic stroke activities

RSC Advances ◽  
2016 ◽  
Vol 6 (43) ◽  
pp. 36888-36897 ◽  
Author(s):  
Yanlin Jian ◽  
Jing Ji ◽  
Zhangjian Huang ◽  
Yang Gao ◽  
Xiao Sheng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Infarct Size ◽  
Water Content ◽  
Neurological Deficit ◽  
Brain Water Content ◽  
Antiplatelet Aggregation ◽  
Preparation And Evaluation ◽  
Brain Water

(R)- and (S)-1 were as potent as racemate 1 in antiplatelet aggregation, antioxidation, reduction of infarct size and brain-water content, as well as neurological deficit.

FGF10 Attenuates Experimental Traumatic Brain Injury through TLR4/MyD88/NF-κB Pathway

2021 ◽  
pp. 1-9
Author(s):  
Qinhan Hou ◽  
Hongmou Chen ◽  
Quan Liu ◽  
Xianlei Yan
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Expression ◽  
Water Content ◽  
Neurological Deficit ◽  
Neuronal Apoptosis ◽  
Neuronal Damage ◽  
Intraventricular Injection ◽  
Brain Water Content ◽  
Brain Water

Traumatic brain injury (TBI) can induce neuronal apoptosis and neuroinflammation, resulting in substantial neuronal damage and behavioral disorders. Fibroblast growth factors (FGFs) have been shown to be critical mediators in tissue repair. However, the role of FGF10 in experimental TBI remains unknown. In this study, mice with TBI were established via weight-loss model and validated by increase of modified neurological severity scores (mNSS) and brain water content. Secondly, FGF10 levels were elevated in mice after TBI, whereas intraventricular injection of Ad-FGF10 decreased mNSS score and brain water content, indicating the remittance of neurological deficit and cerebral edema in TBI mice. In addition, neuronal damage could also be ameliorated by stereotactic injection of Ad-FGF10. Overexpression of FGF10 increased protein expression of Bcl-2, while it decreased Bax and cleaved caspase-3/PARP, and improved neuronal apoptosis in TBI mice. In addition, Ad-FGF10 relieved neuroinflammation induced by TBI and significantly reduced the level of interleukin 1β/6, tumor necrosis factor α, and monocyte chemoattractant protein-1. Moreover, Ad-FGF10 injection decreased the protein expression level of Toll-like receptor 4 (TLR4), MyD88, and phosphorylation of NF-κB (p-NF-κB), suggesting the inactivation of the TLR4/MyD88/NF-κB pathway. In conclusion, overexpression of FGF10 could ameliorate neurological deficit, neuronal apoptosis, and neuroinflammation through inhibition of the TLR4/MyD88/NF-κB pathway, providing a potential therapeutic strategy for brain injury in the future.

Gv20-Based Acupuncture for Animal Models of Acute Intracerebral Haemorrhage: A Preclinical Systematic Review and Meta-Analysis

2014 ◽  
Vol 32 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Hui-qin Li ◽  
Ji-huang Li ◽  
Ai-ju Liu ◽  
Mai-yun Ye ◽  
Guo-qing Zheng
Keyword(s):  
Animal Models ◽  
Water Content ◽  
Intracerebral Haemorrhage ◽  
Neurological Deficit ◽  
Meta Analysis ◽  
Acupuncture Point ◽  
Brain Water Content ◽  
Global Estimate ◽  
Item Checklist ◽  
Brain Water

Background Spontaneous intracerebral haemorrhage (ICH) is the most devastating subtype of stroke, but there is currently no evidence-based treatment strategy. Acupuncture is a well-known traditional Chinese therapy for stroke-induced disability, and GV20 is the commonly used acupuncture point. Objective To evaluate the efficacy of GV20-based acupuncture in animal models of acute ICH. Methods Studies of GV20-based acupuncture in animal models of acute ICH were identified from six databases up to July 2013. Study quality for each included article was evaluated according to the CAMARADES 10-item checklist. Outcome measures were neurological deficit scores and brain water content. All the data were analysed using RevMan V.5.1 software. Results Nineteen studies were identified describing procedures involving 1628 animals. The quality score of the studies ranged from 3 to 6, with a mean of 4.6. The global estimate of the effect of GV20-based acupuncture was 0.19 (95% CI 0.13 to 0.25, p<0.001) SDs improvement in outcome compared with controls. In subgroup analyses, size of effect was higher where the outcome was measured as the neurological deficit score than the brain water content or both (p<0.001). Conclusions These findings show the possible efficacy of GV20-based acupuncture in animal models of acute ICH, suggesting it as a candidate therapy for acute ICH.

scholarly journals Parthenolide Is Neuroprotective in Rat Experimental Stroke Model: Downregulating NF-κB, Phospho-p38MAPK, and Caspase-1 and Ameliorating BBB Permeability

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Lipeng Dong ◽  
Huimin Qiao ◽  
Xiangjian Zhang ◽  
Xiaolin Zhang ◽  
Chaohui Wang ◽  
...  
Keyword(s):  
Western Blot ◽  
Water Content ◽  
Brain Tissue ◽  
Neurological Deficit ◽  
Infarct Volume ◽  
Brain Water Content ◽  
Ischemic Brain ◽  
Caspase 1 ◽  
Ischemic Brain Tissue ◽  
Brain Water

Inflammatory damage plays an important role in cerebral ischemic pathogenesis and may represent a target for treatment. Parthenolide (PN) has been proved to elicit a wide range of biological activities through its anti-inflammatory action in the treatment of migraine, arthritis, and atherosclerosis. To decide whether this effect applies to ischemic injury in brain, we therefore investigate the potential neuroprotective role of PN and the underlying mechanisms. Male Sprague-Dawley rats were randomly divided into Saline, Vehicle, and PN groups and a permanent middle cerebral artery occlusion (MCAO) model was used. PN administered intraperitoneally immediately after cerebral ischemia and once daily on the following days. At time points after MCAO, neurological deficit, infarct volume, and brain water content were measured. Immunohistochemistry, western blot and RT-PCR were used to analyze the expression of NF-κB and caspase-1 in ischemic brain tissue. Phospho-p38MAPK and claudin-5 were detected by western blot. The results indicated that PN dramatically ameliorated neurological deficit, brain water content, and infarct volume, downregulated NF-κB, phospho-p38MAPK, and caspase-1 expressions, and upregulated claudin-5 expression in ischemic brain tissue.Conclusions.PN protected the brain from damage caused by MCAO; this effect may be through downregulating NF-κB, phosho-p38MAPK, and caspase-1 expressions and ameliorating BBB permeability.

scholarly journals L-3-n-butylphthalide protect the neuro by reducing inflammation and brain edema in rat intracerebral hemorrhage model

2019 ◽  
Author(s):  
Zhou Zeng ◽  
Xiyu Gong ◽  
Zhiping Hu
Keyword(s):  
Ischemic Stroke ◽  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Vehicle Group ◽  
Brain Water Content ◽  
Tnf Α ◽  
Brain Barrier Permeability ◽  
Brain Water

Abstract Background：Previous studies have shown that L-3-n-butylphthalide(NBP), which is a compound found in Apium graveolens Linn seed extracts, could have neuroprotective effects on acute ischemic stroke through anti-inflammation and by reducing brain edema. The pathological inflammatory pathways and consequent brain edema in intracerebral hemorrhage (ICH) share some characteristics with ischemic stroke. Methods：We hypothesized that NBP has anti-inflammatory and therapeutic effects on rats with ICH. ICH was induced by an infusion of bacterial collagenase type IV into the unilateral striatum of anesthetized rats. The therapeutic effect of NBP was measured by assessing neurological function, brain water content, blood-brain barrier permeability, and expression of tumor necrosis factor-alpha (TNF-α) and matrix metalloproteinase-9 (MMP-9) around the hematoma 48 hours after surgery. Magnetic resonance imaging (MRI) was performed 4 and 48 hours after ICH induction, and ICH-induced injured area volumes were measured using T2-weighted images. Results： The NBP treatment group performed better in the neurological function test than the vehicle group. Moreover, in comparison with the vehicle group, NBP group showed a lower expanded hematoma volume, brain water content, blood-brain barrier permeability, and TNF-α/ MMP-9 expression level. Conclusions：Our results suggested that NBP have a neuroprotective effect by reducing inflammation and brain edema in rat ICH model. Therefore, our findings also show the potential for clinical application of NBP in the treatment of ICH.

Abstract WMP24: Quantitative Relaxometry Quantifies Brain Edema After Ischemic Stroke

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Thomas W Battey ◽  
Iris Y Zhou ◽  
Ann-Christin U Ostwaldt ◽  
Takahiro Igarashi ◽  
Philip Z Sun ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Water Content ◽  
Brain Edema ◽  
Signal Intensity ◽  
Proton Density ◽  
Lesion Volume ◽  
Brain Water Content ◽  
T1 And T2 ◽  
Swelling Volume ◽  
Brain Water

Introduction: Brain edema is an adverse complication of ischemic stroke, and is associated with substantial morbidity and mortality. We investigated whether relaxometry parameters of MRI are a reliable measure of brain edema in an animal model. Hypothesis: We hypothesize that quantitative relaxometry parameters of MRI in a rat model of stroke tightly correlate with brain edema. Methods: We permanently occluded the middle cerebral artery of 18 rats using the filament occlusion method. Fifteen surviving animals were imaged at 48 hours with a Bruker 4.7 T MRI scanner with Diffusion-weighted imaging (DWI), T1 and T2 maps, and proton-density weighted (PDW) imaging. Hemispheric and lesional volumes were generated on DWI. For quantitative T1, quantitative T2 and PDW images, signal intensity values relative to the contralateral hemisphere were determined. The percent water content in the rat brain was measured using the wet-dry method. Additional volumetric measurements of swelling were calculated based on hemisphere volumes determined on MRI. Correlation testing and logistic regression was performed to assess the relationship between imaging measures and swelling. Results: The mean lesion volume was 352 mm3. Brain water content and swelling volume were closely associated (r=0.80, p<0.001). PDW, T1 and T2 ratios highly correlated with brain water content (r=0.91, p<0.0001, r=0.94, p<0.0001 and r=0.97, p<0.0001, respectively). Ratios for PDW, T1 and T2 were also associated with swelling volume (r=0.67, p<0.0063, r=0.73, p<0.0022, and r=0.74, p<0.0017). Conclusion: Signal intensity ratios derived from PDW as well as quantitative T1 and T2 MRI can be leveraged to quantify brain water content and brain edema. These measures are useful markers for edema quantification that can be applied to any condition that leads to brain edema in both animal models and human patients.

scholarly journals Ulinastatin alleviates traumatic brain injury by reducing endothelin-1

2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Water Content ◽  
Brain Edema ◽  
Rat Model ◽  
Neurosurgical Procedures ◽  
Brain Water Content ◽  
The Brain ◽  
Brain Water

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.

scholarly journals Quantitation of Photochemically Induced Focal Cerebral Ischemia in the Rat

1988 ◽  
Vol 8 (1) ◽  
pp. 89-95 ◽  
Author(s):  
John J. Grome ◽  
Gerlinde Gojowczyk ◽  
Wolfgang Hofmann ◽  
David I. Graham
Keyword(s):  
Cerebral Ischemia ◽  
Water Content ◽  
Rose Bengal ◽  
Tissue Damage ◽  
Focal Cerebral Ischemia ◽  
Ischemic Damage ◽  
Brain Water Content ◽  
Ischemic Insult ◽  
Ischemic Lesion ◽  
Brain Water

This study was carried out with a recently developed model of focal cerebral ischemia in the rat based on the photochemical induction of thrombotic stroke using the dye Rose Bengal. We examined the change in the volume of the lesion and brain water content, in separate groups of rats, at different times (1, 4, 24, 72, and 168 h) after the induction of the ischemic lesion. The volume of ischemic damage increased rapidly between 1 and 24 h after the ischemic insult and decreased between 24 and 168 h. The lesion at 168 h was significantly larger than that following 1 h of ischemia and similar to that obtained at 4 h, suggesting that the maximum extent of tissue damage (without the involvement of significant edema) was reached within the first 4 h in this model. The enlargement of the lesion after 4 h correlated closely with changes in brain water content.

scholarly journals Glucose Intolerance Induced by Oligemic Brain Hypoxia: The Effect of Terguride

1997 ◽  
Vol 40 (3) ◽  
pp. 57-60
Author(s):  
Věroslav Golda ◽  
Jiřina Hilgertová
Keyword(s):  
Glucose Tolerance ◽  
Water Content ◽  
Glucose Intolerance ◽  
Insulin Binding ◽  
Tolerance Test ◽  
Female Rats ◽  
Brain Water Content ◽  
Brain Hypoxia ◽  
Series Of Experiments ◽  
Brain Water

Two series of experiments were performed. In the first one experiments were carried out in Koletsky genetically hypertensive lean female rats and in the normotensive female rats of Wistar strain. Glucose intolerance was induced by oligemic brain hypoxia (4 hours of occlusion of both common carotid arteries followed by 44 hours reperfusion). Brain water content were used as a marker of brain edema.Changes in insulinemia and specific insulin binding were used as expression of regulative mechanisms participating in modification of glucose tolerance. The effect of terguride (trans-dihydro- lisuride) was tested.Brain hypoxia induced glucose intolerance in both strains of rat but brain edema was found only in the normotensive females. Both abnormalities were alleviated by terguride treatment. Basal glycaemia was not changed either by the brain hypoxia or by terguride treatment,except normoternsive female where brain hypoxia induced hyperglycaemia. The second series of experiments were carried out in the normotensive females. The arrangement of experiments was the same as in first series except omission of the final glucose tolerance test. Brain hypoxia causes increase in brain water content. The mentioned elevation of brain water content was alleviated by terguride treatmnet. Insulin binding to erythrocytes was not influenced by brain hypoxia. Terguride treatment shows decrease of insulin binding to erythrocytes. Brain hypoxia elevates insulinemia which was not alleviated by terguride treatment.

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