Neuroprotective Effects of Xanthohumol, a Prenylated Flavonoid from Hops (Humulus lupulus), in Ischemic Stroke of Rats

2012 ◽  
Vol 60 (8) ◽  
pp. 1937-1944 ◽  
Author(s):  
Ting-Lin Yen ◽  
Chung-King Hsu ◽  
Wan-Jung Lu ◽  
Cheng-Ying Hsieh ◽  
George Hsiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Humulus Lupulus ◽  
Neuroprotective Effects

Heat Shock Protein 70 kDa as a Target for Diagnostics and Therapy of Cardiovascular and Cerebrovascular Diseases

2019 ◽  
Vol 25 (6) ◽  
pp. 710-714 ◽  
Author(s):  
Ekaterina V. Konstantinova ◽  
Natalia S. Chipigina ◽  
Marina H. Shurdumova ◽  
E.I. Kovalenko ◽  
Alexander M. Sapozhnikov
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Stroke ◽  
Heat Shock ◽  
Cerebrovascular Diseases ◽  
Peripheral Blood Lymphocytes ◽  
Neuroprotective Effects ◽  
Adverse Conditions ◽  
Shock Proteins ◽  
Diagnostics And Therapy ◽  
Main Factor

Acute focal ischemia is a main factor of pathogenesis of a number of widespread cardiovascular and cerebrovascular diseases, in particular, myocardial infarction and ischemic stroke. It is known that under the conditions of ischemia expression of intracellular heat shock proteins (HSPs), especially HSP70, grows greatly irrespective of the cell type. This stress-induced cell response is connected with cytoprotective properties of HSP70. The protective functions of HSP70 contribute to the cell survival under adverse conditions and inhibit development of programmed cell death. It was shown, that the level of HSP70 increases in cardiomyocytes and brain cells in response to ischemia, that was connected with cardioprotective and neuroprotective effects. Besides, in recent years, clinical studies of HSP70 have demonstrated elevated level of HSP70 in peripheral blood lymphocytes in groups of patients with ischemic stroke and myocardial infarction. This review indicates that HSP70 can serve as a target for developing new approaches to diagnostics and therapy of cardiovascular and cerebrovascular diseases.

scholarly journals The Effects ofChunghyul-Dan(A Korean Medicine Herbal Complex) on Cardiovascular and Cerebrovascular Diseases: A Narrative Review

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Woo-Sang Jung ◽  
Seungwon Kwon ◽  
Seung-Yeon Cho ◽  
Seong-Uk Park ◽  
Sang-Kwan Moon ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Ethanol Extract ◽  
Inhibitory Effect ◽  
Cerebrovascular Diseases ◽  
Stroke Recurrence ◽  
Neuroprotective Effects ◽  
Clinical Safety ◽  
Endogenous Catecholamine ◽  
Rhei Rhizoma ◽  
Coa Reductase

Chunghyul-dan(CHD) is a herbal complex containing 80% ethanol extract and is composed ofScutellariae Radix,Coptidis Rhizoma,Phellodendri Cortex,Gardeniae Fructus, andRhei Rhizoma. We have published several experimental and clinical research articles on CHD. It has shown antilipidemic, antihypertensive, antiatherosclerotic, and inhibitory effects on ischemic stroke recurrence with clinical safety in the previous studies. The antilipidemic effect of CHD results from 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and pancreatic lipase-inhibitory activity. The antihypertensive effect likely results from the inhibitory effect on endogenous catecholamine(s) release and harmonization of all components showing the antihypertensive effects. Furthermore, anti-inflammatory and antioxidant effects on endothelial cells are implicated to dictate the antiatherosclerotic effects of CHD. It also showed neuroprotective effects on cerebrovascular and parkinsonian models. These effects of CHD could be helpful for the prevention of the recurrence of ischemic stroke. Therefore, we suggest that CHD could be a promising medication for treating and preventing cerebrovascular and cardiovascular diseases. However, to validate and better understand these findings, well-designed clinical studies are required.

Abstract TMP46: Is There an Effect of Statins on Ischemic Stroke Functional Outcomes in the Oldest Old?

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Matthew Alcusky ◽  
Anne L Hume ◽  
Kate L Lapane
Keyword(s):  
Ischemic Stroke ◽  
Functional Status ◽  
Functional Outcomes ◽  
Acute Treatment ◽  
Functional Dependence ◽  
Oldest Old ◽  
Health Benefit ◽  
Neuroprotective Effects ◽  
Data Set ◽  
Statin Use

Background: The net health benefit of statin use in the oldest patients remains controversial. Preclinical models and previous clinical studies have suggested statins may exhibit neuroprotective effects in stroke, however evidence in the very old remains limited. Our objective was to compare changes in functional status before and after acute ischemic stroke (AIS) between statin users and non-users in a national cohort. Methods: A patient’s first hospitalization for AIS from 04/01/11 to 12/31/2012 was selected from Medicare Part A claims. Patients with a pre-hospitalization nursing home Minimum Data Set assessment and a post-hospitalization assessment in a skilled nursing facility were included. Pre-stroke statin exposure was defined using Part D claims. Functional status was measured continuously and categorically (dependent:<20, partially dependent(PD):20-59, assisted independent(AI):60-100) using Shah’s modified Barthel Index (mBI). Multivariable logistic regression examined the association of statins with a minimum clinically important mBI decrease of 10 points among non-dependent patients. Results: Among 10,203 patients with an assessment before hospitalization, 7.2% died, and 48.7% were included (mean age: 83.6±9.6; 74.5% women). Statin use was common (36.5%), while acute treatment was infrequent (thrombolysis: 4.9%; thrombectomy: 0.1%). The distribution of functional dependence, PD, and AI shifted from 17.3%, 56.1%, and 26.7% at baseline to 49.7%, 44.4%, and 5.9% post-stroke, respectively. A consistent association with 10-point mBI decline was observed for statin exposure among all non-dependent (OR: 0.8; 95%CI: 0.7-1.0) and within strata of PD (OR:0.8; 95%CI: 0.7-1.0) and AI patients (OR: 0.8; 95%CI: 0.5-1.3). In contrast, acute treatment was more strongly associated with function in AI (OR: 0.5; 95%CI: 0.2-1.0) versus PD patients (OR: 1.0; 95%CI: 0.7-1.5). Conclusion: In this high-burden population, our results are suggestive of a possible protective association for pre-stroke statin exposure. Further research is needed to examine temporal and dose-response relationships between statin exposure and functional outcomes across diverse patient populations.

Protective effects of the angiotensin II AT2 receptor agonist compound 21 in ischemic stroke: a nose-to-brain delivery approach

2018 ◽  
Vol 132 (5) ◽  
pp. 581-593 ◽  
Author(s):  
Douglas M. Bennion ◽  
Chad H. Jones ◽  
Alex N. Dang ◽  
Jacob Isenberg ◽  
Justin T. Graham ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Angiotensin Ii ◽  
Receptor Agonist ◽  
At2 Receptor ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Receptor Agonists ◽  
Compound 21 ◽  
Neuroprotective Actions

Significant neuroprotective effects of angiotensin II type 2 (AT2) receptor (AT2 receptor) agonists in ischemic stroke have been previously demonstrated in multiple studies. However, the routes of agonist application used in these pre-clinical studies, direct intracerebroventricular (ICV) and systemic administration, are unsuitable for translation into humans; in the latter case because AT2 receptor agonists are blood–brain barrier (BBB) impermeable. To circumvent this problem, in the current study we utilized the nose-to-brain (N2B) route of administration to bypass the BBB and deliver the selective AT2 receptor agonist Compound 21 (C21) to naïve rats or rats that had undergone endothelin 1 (ET-1)-induced ischemic stroke. The results obtained from the present study indicated that C21 applied N2B entered the cerebral cortex and striatum within 30 min in amounts that are therapeutically relevant (8.4–9 nM), regardless of whether BBB was intact or disintegrated. C21 was first applied N2B at 1.5 h after stroke indeed provided neuroprotection, as evidenced by a highly significant, 57% reduction in cerebral infarct size and significant improvements in Bederson and Garcia neurological scores. N2B-administered C21 did not affect blood pressure or heart rate. Thus, these data provide proof-of-principle for the idea that N2B application of an AT2 receptor agonist can exert neuroprotective actions when administered following ischemic stroke. Since N2B delivery of other agents has been shown to be effective in certain human central nervous system diseases, the N2B application of AT2 receptor agonists may become a viable mode of delivering these neuroprotective agents for human ischemic stroke patients.

scholarly journals Neuroprotective effects of long noncoding RNAs involved in ischemic postconditioning after ischemic stroke

2022 ◽  
Vol 17 (6) ◽  
pp. 1299
Author(s):  
Jian-Hui Guo ◽  
Li-Yan Li ◽  
Wei Ma ◽  
Chun-Yan Li ◽  
Si-Jia Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Ischemic Postconditioning ◽  
Neuroprotective Effects

scholarly journals Replicating infant astrocyte behavior in the adult after brain injury improves outcomes

2020 ◽  
Author(s):  
Leon Teo ◽  
Anthony G. Boghdadi ◽  
Jihane Homman-Ludiye ◽  
Iñaki Carril-Mundiñano ◽  
William C. Kwan ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Brain Injuries ◽  
Adult Patients ◽  
Long Term Outcomes ◽  
Neuroprotective Effects ◽  
Age Dependent ◽  
Underlying Mechanisms ◽  
Glial Scarring

AbstractInfants and adults respond differently to brain injuries. Specifically, improved neuronal sparing along with reduced astrogliosis and glial scarring often observed earlier in life, likely contributes to improved long-term outcomes. Understanding the underlying mechanisms could enable the recapitulation of neuroprotective effects, observed in infants, to benefit adult patients after brain injuries. We reveal that in primates, Eph/ ephrin signaling contributes to age-dependent reactive astrocyte behavior. Ephrin-A5 expression on astrocytes was more protracted in adults, whereas ephrin-A1 was associated only with infant astrocytes. Furthermore, ephrin-A5 exacerbated major hallmarks of astrocyte reactivity via EphA2 and EphA4 receptors, which was subsequently alleviated by ephrin-A1. Rather than suppressing reactivity, ephrin-A1 signaling shifted astrocytes towards GAP43+ neuroprotection, accounting for improved neuronal sparing in infants. Reintroducing ephrin-A1 after middle-aged ischemic stroke significantly attenuated glial scarring, improved neuronal sparing and preserved circuitry. Therefore, beneficial infant mechanisms can be recapitulated in adults to improve outcomes after CNS injuries.

scholarly journals Privileged Quinolylnitrones for the Combined Therapy of Ischemic Stroke and Alzheimer’s Disease

2021 ◽  
Vol 14 (9) ◽  
pp. 861
Author(s):  
José M. Alonso ◽  
Alejandro Escobar-Peso ◽  
Alejandra Palomino-Antolín ◽  
Daniel Diez-Iriepa ◽  
Mourad Chioua ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Ischemic Stroke ◽  
Cortical Neurons ◽  
Combined Therapy ◽  
Glucose Deprivation ◽  
Dual Therapy ◽  
Amyloid Peptide ◽  
Neuroprotective Effects ◽  
Number Of Patients

Cerebrovascular diseases such as ischemic stroke are known to exacerbate dementia caused by neurodegenerative pathologies such as Alzheimer’s disease (AD). Besides, the increasing number of patients surviving stroke makes it necessary to treat the co-occurrence of these two diseases with a single and combined therapy. For the development of new dual therapeutic agents, eight hybrid quinolylnitrones have been designed and synthesized by the juxtaposition of selected pharmacophores from our most advanced lead-compounds for ischemic stroke and AD treatment. Biological analyses looking for efficient neuroprotective effects in suitable phenotypic assays led us to identify MC903 as a new small quinolylnitrone for the potential dual therapy of stroke and AD, showing strong neuroprotection on (i) primary cortical neurons under oxygen–glucose deprivation/normoglycemic reoxygenation as an experimental ischemia model; (ii), neuronal line cells treated with rotenone/oligomycin A, okadaic acid or β-amyloid peptide Aβ25–35, modeling toxic insults found among the effects of AD.

Neuroprotection via AT2 receptor agonists in ischemic stroke

2018 ◽  
Vol 132 (10) ◽  
pp. 1055-1067 ◽  
Author(s):  
Douglas M. Bennion ◽  
U. Muscha Steckelings ◽  
Colin Sumners
Keyword(s):  
Ischemic Stroke ◽  
Neuronal Damage ◽  
Recombinant Tissue Plasminogen Activator ◽  
Neurological Deficits ◽  
At2 Receptor ◽  
Neuroprotective Effects ◽  
Receptor Agonists ◽  
Stroke Epidemiology ◽  
The Brain

Stroke is a devastating disease that afflicts millions of people each year worldwide. Ischemic stroke, which accounts for ~88% of cases, occurs when blood supply to the brain is decreased, often because of thromboembolism or atherosclerotic occlusion. This deprives the brain of oxygen and nutrients, causing immediate, irreversible necrosis within the core of the ischemic area, but more delayed and potentially reversible neuronal damage in the surrounding brain tissue, the penumbra. The only currently approved therapies for ischemic stroke, the thrombolytic agent recombinant tissue plasminogen activator (rtPA) and the endovascular clot retrieval/destruction processes, are aimed at restoring blood flow to the infarcted area, but are only available for a minority of patients and are not able in most cases to completely restore neurological deficits. Consequently, there remains a need for agents that will protect neurones against death following ischemic stroke. Here, we evaluate angiotensin II (Ang II) type 2 (AT2) receptor agonists as a possible therapeutic target for this disease. We first provide an overview of stroke epidemiology, pathophysiology, and currently approved therapies. We next review the large amount of preclinical evidence, accumulated over the past decade and a half, which indicates that AT2 receptor agonists exert significant neuroprotective effects in various animal models, and discuss the potential mechanisms involved. Finally, after discussing the challenges of delivering blood–brain barrier (BBB) impermeable AT2 receptor agonists to the infarcted areas of the brain, we summarize the evidence for and against the development of these agents as a promising therapeutic strategy for ischemic stroke.

Abstract TMP48: Effect of Pre-Morbid Antianxiety and Antidepressant Medications on Ischemic Stroke Functional Outcome

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Cecilia Peterson ◽  
Ka-Ho Wong ◽  
Michael Dela Cruz ◽  
Kirby Taylor ◽  
Jennifer J Majersik ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Regression Models ◽  
Primary Outcome ◽  
Negative Impact ◽  
Secondary Analysis ◽  
Anxiety And Depression ◽  
Neuroprotective Effects ◽  
Logistic Regression Models ◽  
Antidepressant Medications

Introduction: Antianxiety and antidepressant medications have shown some neuroprotective effects following stroke. However, the effect of premorbid use of these medications remains unclear. Hypothesis: Pre-morbid exposure to antianxiety or antidepressant medications will negatively impact recovery from acute ischemic stroke, measured by modified Rankin scale (mRS) at 90 days after stroke onset. Methods: This is a secondary analysis of the Albumin in Acute Ischemic Stroke (ALIAS) 2 trial. The primary outcome is 90-day mRS 0-1. The exposure is premorbid antidepressant or antianxiety medication. We fit univariate and multivariate logistic regression models to our outcome, with covariates chosen using a stepwise backwards interactive selection. Results: We included 806 patients with a mean (SD) age of 64.4 (12.8) years. The median (IQR) NIH Stroke Scale was 11 (8, 17) and 54.3% were male, 75.6% were Caucasian, 88.8% received tPA, 72.5% had hypertension, and 20.3% had diabetes. A total of 140/806 (17.4%) of patients took either an antidepressant or antianxiety medication, of which 91 took an antidepressant, 34 took an antianxiety medication, and 15 took both. The median (IQR) mRS Scale was one point higher in patients on antidepressant or antianxiety medication pre-stroke (3 vs. 2, p=0.019). The primary outcome of mRS 0-1 was seen in 37.7% of all patients. Taking an antidepressant or antianxiety medication was associated with lower odds of a good outcome in univariate (OR 0.61, 95% CI 0.41-0.91, p=0.015) and multivariate models (aOR 0.62, 95% CI 0.40-0.95, p=0.027) (Table 1). Conclusion: Pre-morbid exposure to antianxiety or antidepressant medications is associated with a worse outcome after acute ischemic stroke. This may be due to a negative impact of pre-stroke anxiety and depression that outweigh any neuroprotective factors of these medications.

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