scholarly journals Electroacupuncture reactivates estrogen receptors to restore the neuroprotective effect of estrogen against cerebral ischemic stroke in long‐term ovariectomized rats

2021 ◽  
Author(s):  
Yulong Ma ◽  
Erlong Niu ◽  
Fei Xie ◽  
Min Liu ◽  
Miao Sun ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Estrogen Receptors ◽  
Neuroprotective Effect ◽  
Ovariectomized Rats ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

scholarly journals Cerebral Ischemic Stroke: is Gender Important?

2013 ◽  
Vol 33 (9) ◽  
pp. 1355-1361 ◽  
Author(s):  
Claire L Gibson
Keyword(s):  
Ischemic Stroke ◽  
Developed Countries ◽  
Cerebral Stroke ◽  
Clinical Investigations ◽  
Neuroprotective Strategies ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Gender Influences ◽  
Gender Specific

Cerebral stroke continues to be a major cause of death and the leading cause of long-term disability in developed countries. Evidence reviewed here suggests that gender influences various aspects of the clinical spectrum of ischemic stroke, in terms of influencing how a patients present with ischemic stroke through to how they respond to treatment. In addition, this review focuses on discussing the various pathologic mechanisms of ischemic stroke that may differ according to gender and compares how intrinsic and hormonal mechanisms may account for such gender differences. All clinical trials to date investigating putative neuroprotective treatments for ischemic stroke have failed, and it may be that our understanding of the injury cascade initiated after ischemic injury is incomplete. Revealing aspects of the pathophysiological consequences of ischemic stroke that are gender specific may enable gender relevant and effective neuroprotective strategies to be identified. Thus, it is possible to conclude that gender does, in fact, have an important role in ischemic stroke and must be factored into experimental and clinical investigations of ischemic stroke.

Abstract P806: Sirtuin1 Plays a Critical Role in Reversing Skeletal Muscle Atrophy in Cerebral Ischemic Stroke

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Junaith S Mohamed ◽  
Peter J Ferrandi ◽  
Paez G Hector ◽  
Christopher R Pitzer ◽  
Stephen E Alway
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Stroke ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Rna Seq ◽  
Stroke Patients ◽  
Post Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Stroke is a leading cause of mortality and long-term disability in patients worldwide. Skeletal muscle is the primary systemic target organ of stroke that severely induces muscle wasting and weakness, which contributes more to the long-term functional disability in stroke patients than any other disease. Currently, no approved pharmacological drug is available to treat stroke-induced muscle loss. Rehabilitative therapy is the only available option to improve muscle function in stroke patients. However, higher muscle fatigability and lower muscle strength from extensive muscle wasting in post-stroke patients provide poor rehabilitative outcomes. As a result, about two-thirds of stroke survivors persist in a state of insufficient recovery and experience physical disability that drastically reduces their health and quality of life. The major challenge in the drug discovery effort for treating post-stroke muscle wasting is the lack of our understanding of the molecular and/or cellular mechanisms that underlie the muscle wasting in stroke. To understand the molecular origin of stroke-induced muscle atrophy, gene expression profiling and associated biological pathway enrichment studies were performed in a mouse model of cerebral ischemic stroke using high-throughput RNA sequencing and extensive bioinformatic analyses. RNA-seq data revealed that the elevated atrophy in skeletal muscle observed in response to stroke was primairly associated with the altered expression of genes involved in the muscle protein degradation pathway. Further analysis of RNA-seq data identified Sirtuin1 (SirT1) as a critical protein that plays a significant role in regulating post-stroke muscle mass. SirT1 gain-of-function in skeletal muscle significantly reversed stroke-induced muscle atrophy via inhibiting the activation of the ubiquitin proteasomal pathway and restoring autophagy function. Collectively, this study identified suppression of SirT1as a novel mechanism by which stroke induces muscle atrophy.

scholarly journals The Neuroprotective Effect of l-Borneolum on Cerebral Ischemic Stroke by Regulating Dll4/Notch1 Pathway

2021 ◽  
Author(s):  
Taiwei Dong ◽  
Nian Chen ◽  
Rong Ma ◽  
Qian Xie ◽  
Xiaoqing Guo ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Neurological Function ◽  
Immunohistochemical Method ◽  
Triphenyltetrazolium Chloride ◽  
Severity Scores ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Abstract Aiml-Borneolum is a monoterpene compound witch deserved from Blumea balsamifera (L.) DC, this study aimed to investigate the potential mechanism of l-borneolum on cerebral ischemic stroke (CIS) rats and provide evidence for the development of l-borneolum in CIS.MethodsPermanent middle cerebral artery occlusion (pMCAO) model rats were applied to this study. Neurological function was assessed by modified neurological severity scores (mNSS) and Longa neurological function scoring methods. The pathological changes of cerebral tissue were evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) and hematoxylin-eosin (HE) staining. Ultrastructure of blood brain barrier (BBB) was observed by transmission electron microscopy. Additionally, the expression of Notch1, Dll4, Hey1, Hes1, Hes5, VEGFA and p65 in the cortex were determined by Western blotting (WB) while expression of caspase 3 were determined by immunohistochemical method (IHC). Resultsl-Borneolum improved neurological function in a dose-dependently. l-Borneolum significantly alleviated brainstem edema and inflammation, as well as improved the ultrastructure of capillary and BBB in cortex. Moreover, 0.2 g/kg l-borneolum substantially decreased the protein expressions of Dll4, Notch1, Hes1, Hes5, and VEGFA in the cortex while decreased the level of Caspase-3 in the cortex of rats. Conclusionsl-Borneolum could repair neurological function by regulating Dll4/Notch1 signaling pathway.

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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