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      Neuroprotective effects of Yiqihuoxue calm wind capsule on ischemic stroke in rats

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          Abstract

          Stroke remains the third leading cause of death and of adult disability worldwide. Vascular occlusion, followed by ischemic cascade, leads to irreversible tissue injury. Recombinant tissue plasminogen activator is the only FDA approved drug for the current treatment of acute ischemic stroke. However, traditional Chinese medicine has a long history and rich clinical experience in the treatment and rehabilitation of ischemic stroke. Using a classical middle cerebral artery occlusion (MCAO) stroke model, we tested the effectiveness of Yiqihuoxue calm wind (YCW) capsule on neurological function, gross pathology and oxidative stress status in MCAO rats. YCW capsule (3.36 and 6.72 g·kg −1 of crude drug) could significantly lower Longa’s score and superoxide dismutase (SOD) level, together with less necrotic cells and infarcted area. In addition to elevated MDA and downregulated iNOS expression, YCW capsule exhibited its neuroprotective effects via free radical scavenging and NO inhibition.

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          Most cited references 18

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          Temporal and spatial dynamics of cerebral immune cell accumulation in stroke.

          Ischemic stroke leads to significant morbidity and mortality in the Western world. Early reperfusion strategies remain the treatment of choice but can initiate and augment an inflammatory response causing secondary brain damage. The understanding of postischemic inflammation is very limited. The objectives of this study were to define the temporal and spatial infiltration of immune cell populations and their activation patterns in a murine cerebral ischemia-reperfusion injury model. Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. Immunohistochemistry and flow cytometry were used to quantify the infiltrating immune cell subsets. Accumulation of microglia and infiltration of the ischemic hemisphere by macrophages, lymphocytes, and dendritic cells (DCs) preceded the neutrophilic influx. DCs were found to increase 20-fold and constituted a substantial proportion of infiltrating cells. DCs exhibited a significant upregulation of major histocompatibility complex II and major histocompatibility complex II high-expressing DCs were found 100 times more abundant than in sham conditions. Upregulation of the costimulatory molecule CD80 was observed in DCs and microglial cells but did not further increase in major histocompatibility complex II high-expressing DCs. No lymphocyte activation was observed. Additionally, regulatory immune cells (natural killer T-cells, CD4(-)/CD8(-)T lymphocytes) cumulated in the ischemic hemisphere. This study provides a detailed analysis of the temporal dynamics of immune cell accumulation in a rodent stroke model. The peculiar activation pattern and massive increase of antigen-presenting cells in temporal conjunction with regulatory cells might provide additional insight into poststroke immune regulation.
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            Acute ischemic stroke: overview of major experimental rodent models, pathophysiology, and therapy of focal cerebral ischemia.

            Ischemic stroke is a devastating disease with a complex pathophysiology. Animal modeling of ischemic stroke serves as an indispensable tool first to investigate mechanisms of ischemic cerebral injury, secondly to develop novel antiischemic regimens. Most of the stroke models are carried on rodents. Each model has its particular strengths and weaknesses. Mimicking all aspects of human stroke in one animal model is not possible since ischemic stroke is itself a very heterogeneous disorder. Experimental ischemic stroke models contribute to our understanding of the events occurring in ischemic and reperfused brain. Major approaches developed to treat acute ischemic stroke fall into two categories, thrombolysis and neuroprotection. Trials aimed to evaluate effectiveness of recombinant tissue-type plasminogen activator in longer time windows with finer selection of patients based on magnetic resonance imaging tools and trials of novel recanalization methods are ongoing. Despite the failure of most neuroprotective drugs during the last two decades, there are good chances to soon have effective neuroprotectives with the help of improved preclinical testing and clinical trial design. In this article, we focus on various rodent animal models, pathogenic mechanisms, and promising therapeutic approaches of ischemic stroke.
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              Neuronal oxidative stress in acute ischemic stroke: sources and contribution to cell injury.

              Oxidative stress has emerged as a key deleterious factor in brain ischemia and reperfusion. Malfunction of the oxidative respiratory chain in mitochondria combines with the activation of cytoplasmic oxidases to generate a burst of reactive oxygen species that cannot be neutralised by the cell's antioxidant mechanisms. As a result, oxidative stress contributes directly to necrosis and apoptosis through a number of pathways in ischemic tissue. Pharmacological intervention with antioxidants or enhancers of endogenous antioxidant molecules is proving to be difficult due to the speed and scope of the oxidative impact. Additionally, the knowledge that neuronal fate in ischemic stroke is tightly linked to other brain cells like endothelial cells and astrocytes has shifted the focus of study from isolated neurons to the neurovascular unit. For this reason, recent efforts have been directed towards understanding the sources of oxidative stress in ischemic stroke and attempting to block the generation of oxygen radicals. Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                CJNM
                Chinese Journal of Natural Medicines
                Elsevier
                1875-5364
                20 October 2017
                : 15
                : 10
                : 758-765
                Affiliations
                1School of Pharmaceutical Science, Zhengzhou University, Zhengzhou 450001, China
                2Department of Pharmacology, Henan Provincial Institute of Food and Drug Control, Zhengzhou 450003, China
                3Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases of Henan Province, Zhengzhou 450001, China
                Author notes
                *Corresponding author: ZHANG Zhen-Zhong, Tel: 6(0)391459567; Fax: 6(0)291459547; E-mail: zhenzhongz@ 123456126.com

                These authors have no conflict of interest to declare.

                Article
                S1875-5364(17)30107-3
                10.1016/S1875-5364(17)30107-3
                Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
                Funding
                Funded by: Henan Science and Technology Innovation Talent project
                Award ID: 144200510028
                This project was supported by Henan Science and Technology Innovation Talent project (No. 144200510028).

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