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Transplantation of human neural stem/progenitor cells overexpressing galectin-1 improves functional recovery from focal brain ischemia in the mongolian gerbil
Junichi Yamane, Satoru Ishibashi, Masanori Sakaguchi, Toshihiko Kuroiwa, Yonehiro Kanemura, Masaya Nakamura, Hiroyuki Miyoshi, Kazunobu Sawamoto, Yoshiaki Toyama, Hidehiro Mizusawa, Hideyuki Okano
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-35
Abstract: Stem cell-based therapies have been performed in various clinical settings, although many lack scientific evidence of their effectiveness [1]. Among stem cell-based therapies, transplantation of human neural stem/progenitor cells (hNSPCs) is relatively well substantiated by peer-reviewed literatures [2-8]. One reason underlying the relative success of hNSPCs-transplantation is its low occurrence of tumor formation, which is a clear advantage compared with transplantation of embryonic stem cells or their derivatives [9]. Therefore, we have been examining hNSPCs-transplantation in various preclinical animal models and have shown that hNSPCs-transplantation enhances functional recovery following brain ischemia [10] and spinal cord injury (SCI) [11].Brain ischemia, which is caused by occlusion of a cerebral artery, leads to focal tissue loss and death of multiple neuronal cell types within and around the ischemic region. Patients with brain ischemia exhibit persistent motor, sensory or cognitive impairments, which have devastating effects on their quality of life. Apart from acute thrombolysis, which can be used in only a minority of cases, there is still no effective treatment to promote functional recovery after brain ischemia.hNSPCs can generate all principle cell types (i.e., neurons, astrocytes and oligodendrocytes) in the brain and therefore have great therapeutic potential in severe neurological diseases, including brain ischemia [6,12], which induce death of various cell types [13,14]. hNSPCs can be propagated in large quantities for long-term without a notable loss of the ability to proliferate and differentiate [15]. Therefore, cultured hNSPCs are a promising cell source to treat brain diseases.We previously showed that transplantation of cultured hNSPCs reduced infarct volume and improved functional prognosis in a rodent model of brain ischemia [10]. In the damaged brains of the model animals, hNSPCs differentiated into mature neurons within the ischemic regi
Prophylactic and therapeutic effect of ginko biloba extract (Egb761) on mortality of intestinal deep ischemia-reperfusion model in rats  [PDF]
Mustafa Ate?,M. Hakan K?ksal,M. Fevzi Celayir,Adil Baykan
Dicle Medical Journal , 2010,
Abstract: Objectives: Ginkgo biloba extract (EGb761) is a standardized form of Ginkgo Biloba plant leaves which have been used by Chines nearly 5000 years and Its’ antioxidant activity is known. In this study we aimed to investigate effect use of EGb761 on mortality in Megison'un deep ischemia reperfusion model of rats.Materials and Methods: 138 male Spraque-Dawley rats were used in this study. The rats were divided into 4 groups: Group I (control group), Group II (deep ischemia-reperfusion group), Group III (Group of prophylaxis and treatment of deep ischemia-reperfusion with EGb 761), Group IV (group of treatment with EGb 761 during deep ischemia). Deep ischemia was applied 30 minutes. Rats were followed-up one week after laparotomy. Differences between numbers of mortality in groups during one week follow-up were compared.Results: Number of died rats in Group I, II, III, and IV during one week follow-up were 2 (7.7%), 22 (61.1%), 6 (13.6%), and 11 (34.3%) respectively. Mortality rate decreased statistically significant with use of EGb761 with pro-phylactic and therapeutic purposes (p<0.001, p<0.028).Conclusion: EGb761's prophylactic and therapeutic benefit on intestinal ischemia reperfusion injury was observed. However, these results should be supported with further biochemical and histopathological studies.
The contribution of low affinity NGF receptor (p75NGFR) to delayed neuronal death after ischemia in the gerbil hippocampus.
Bagum MA,Miyamoto O,Toyoshima T,Masada T
Acta Medica Okayama , 2001,
Abstract: The implication of low affinity nerve growth factor receptor (p75NGFR), which is believed to play a pro-apoptotic role, in delayed neuronal death (DND) after ischemia in the gerbil hippocampus was investigated. Immunohistochemistry and Western blot analysis revealed that the presence of p75 NGFR immunoreactivity (IR) was negligible in the hippocampus of the sham control gerbil but appeared clearly in CA1 neurons 3 and 4 days after 5-min transient ischemia. Terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) positive nuclei appeared when the level of p75NGFR IR increased. Furthermore, almost all TUNEL-positive CA1 neurons also costained for p75NGFR. These results suggest that p75NGFR contributes to DND after ischemia by an apoptotic mechanism.
Neuroprotective Effects of Sesamin and Sesamolin on Gerbil Brain in Cerebral Ischemia  [cached]
Fu-Chou Cheng,Tzyy-Rong Jinn,Rolis C.W.Hou,Jason T.C.Tzen
International Journal of Biomedical Science , 2006,
Abstract: Sesamin and sesamolin, abundant lignans found in sesame oil, have been demonstrated to possess several bioactivities beneficial for human health. Excess generation of nitric oxide in lipopolysaccharide-stimulated rat primary microglia cells was significantly attenuated when they were pretreated with sesamin or sesamolin. The neuroprotective effect of sesamin and sesamolin was also observed in vivo using gerbils subjected to a focal cerebral ischemia induced by occlusion of the right common carotid artery and the right middle cerebral artery. Repeated treatment of sesamin or a crude sesame oil extract containing both sesamin and sesamolin significantly reduced the infarct size, visualized via 2,3,5-triphenyltetrazolium chloride staining, by approximately 50% when compared with the control group. These results suggest that sesamin and sesamolin exert effective neuroprotection against cerbral ischemia.
Effects of Enoant and Ischemia and Reperfusion on Lens Metabolites of Rats  [PDF]
Hülya Güngel,Asiye Nurten,?hsan Kara,Serife Evrim Kepekci Tekkeli,Elif ?zk?k,Bur?in Y?ld?z
ISRN Analytical Chemistry , 2013, DOI: 10.1155/2013/964601
Abstract: The effects of the ischemia and reperfusion on the lens metabolites and the effect of a phytotherapeutic commercial product called “Enoant” (mixed polyphenol content) on the selected lens metabolites were investigated. For this aim, 30 Wistar rats were divided into three groups according to their diet and being subjected to ischemia. 10 of the rats as Group I were fed on dry diet; the other 10 (Group II) were fed on dry diet and drinking water with Enoant. At the end of 15 days period, both groups of rats were subjected to ischemia for 2 hours and reperfused. After another 15 days with their same diet, the rats were decapitated. The remaining 10 rats, which were not subjected to ischemia (Group III), were fed on dry diet only. 1HNMR spectroscopy was used for the determination of lens metabolites of each group of rats. The results obtained from the three groups have been compared statistically. The differences of metabolites were significant except pyruvate and succinate. Oral administration of Enoant revealed effects on increasing membrane stabilization, the antioxidant capacity, osmotic regulator molecule capacity, and sorbitol content of lens disturbed by ischemia. Enoant can be used where oxidative or osmotic stress is formed. 1. Introduction As a necessity of life, the oxidative occurrences in cells cause the formation of reactive oxygen species (ROS) and are neutralized in lens through enzymatic or nonenzymatic means [1–3]. The insuffiencies in antioxidative systems induce production of several inflammatory proteins which contribute to the process of cells that promote damage to lipids, DNA, carbohydrates, and proteins. ROS or free oxygen radicals stimulate cataract development. There are a large number of published items related to antioxidants that inhibit the development of cataract [4]. High plants contain flavones that adsorb free oxygen radicals and carry anti-inflammatory characteristics, and they also contain proanthocyanin and other polyphenolic compounds. Proanthocyanin have been reported to inhibit lipid peroxidation, platelet aggregation, and capillary permeability and fragility and to modulate the enzyme of systems including cyclooxygenase and lipoxygenase [5, 6]. They may prevent free radical-mediated cytotoxicity and lipid peroxidation and protect low-density lipoproteins from oxidation [7]. Grape seed, grape juice, and wine are rich in these polyphenolic compounds. Resveratrol, quercetin, and catechin have recently been shown to have activity against oxidative stress. Flavones in the form of pure matter have been known to have
Animal models of focal brain ischemia
Kenneth M Sicard, Marc Fisher
Experimental & Translational Stroke Medicine , 2009, DOI: 10.1186/2040-7378-1-7
Abstract: Stroke is the third leading cause of death and a major cause of disability in the United States [1,2]. Each year, there are approximately 731,000 new strokes and half of the survivors suffer from permanent handicap [3]. Stroke costs the United States approximately $50 billion annually in direct and indirect costs [4]. Given these facts, stroke is a major public health issue requiring urgent development of effective therapies: experimental models of focal brain ischemia help in achieving this goal.80% of human strokes are ischemic in origin [2]. Thus, experimental models of focal cerebral ischemia have been developed in an attempt to closely mimic the changes that occur during and after human ischemic stroke. These models are used to discover the mechanisms involved in the evolution of ischemic injury which, in turn, can lead to the development of novel therapeutic strategies for stroke. These same animal models can then be used to test the safety and efficacy of these treatments in vivo.Most human ischemic strokes are caused by occlusion of the middle cerebral artery (MCA) [5] and so animal models were developed to induce ischemia in this arterial territory. These models aim to satisfy the following criteria: (1) to mimic the pathophysiological changes found in human stroke, (2) to create reproducible lesions, (3) to employ procedures that are relatively simple and noninvasive, (4) to be of low financial cost, and (5) to enable monitoring of physiologic parameters and analysis of brain tissue for outcome measures [6].Many higher animal species fulfill the aforementioned stroke modeling criteria; however, rats are the most commonly used animals for several reasons, including: (1) their resemblance to humans in their cerebral anatomy and physiology, (2) their small size which enables easy analysis of physiology and brain tissue, (3) their low cost, (4) the remarkable genetic homogeneity within strains, and (5) greater public and institutional ethical acceptability of
Study of αB-Crystallin Expression in Gerbil BCAO Model of Transient Global Cerebral Ischemia  [PDF]
Ting Li,Xiaoye Mo,Zheng Jiang,Wenfang He,Wei Lu,He Zhang,Jie Zhang,Liuwang Zeng,Binbin Yang,Han Xiao,Zhiping Hu
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/945071
Abstract: αB-crystallin (α-BC), the fifth member of mammalian small heat shock protein family (HspB5), is known to be expressed in many tissues and has a distinctive interaction with cytoskeleton components. In this study, we investigated that α-BC and microtubule-associated protein-2 (MAP-2), a neuron-specific cytoskeleton protein, were coexpressed in neurons of Gerbil cortex, while in subcortex Gerbil brains, we found that several MAP-2-negative glia cells also express α-BC. When subjected to 10-minute bilateral carotid artery occlusion (BCAO), an increment was observed in α-BC-positive cells after 6-hour reperfusion and peaked at around 7 days after. In the same circumstances, the number and the staining concentration of MAP-2 positive neurons significantly decreased immediately after 6-hour reperfusion, followed by a slow recovery, which is consistent with the increase of α-BC. Our results suggested that α-BC plays an important role in brain ischemia, providing the early protection of neurons by giving intracellular supports through the maintenance of cytoskeleton and extracellular supports through the protection of glia cells.
Study of αB-Crystallin Expression in Gerbil BCAO Model of Transient Global Cerebral Ischemia  [PDF]
Ting Li,Xiaoye Mo,Zheng Jiang,Wenfang He,Wei Lu,He Zhang,Jie Zhang,Liuwang Zeng,Binbin Yang,Han Xiao,Zhiping Hu
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/945071
Abstract: αB-crystallin (α-BC), the fifth member of mammalian small heat shock protein family (HspB5), is known to be expressed in many tissues and has a distinctive interaction with cytoskeleton components. In this study, we investigated that α-BC and microtubule-associated protein-2 (MAP-2), a neuron-specific cytoskeleton protein, were coexpressed in neurons of Gerbil cortex, while in subcortex Gerbil brains, we found that several MAP-2-negative glia cells also express α-BC. When subjected to 10-minute bilateral carotid artery occlusion (BCAO), an increment was observed in α-BC-positive cells after 6-hour reperfusion and peaked at around 7 days after. In the same circumstances, the number and the staining concentration of MAP-2 positive neurons significantly decreased immediately after 6-hour reperfusion, followed by a slow recovery, which is consistent with the increase of α-BC. Our results suggested that α-BC plays an important role in brain ischemia, providing the early protection of neurons by giving intracellular supports through the maintenance of cytoskeleton and extracellular supports through the protection of glia cells. 1. Introduction αB-crystallin/HspB5 (α-BC) is one member of the mammalian small heat shock protein family which consists of ten known members from HspB1 to B10. Though isolated from the crystallin lens, it has been described in a broad number of tissues and organs including the brain, skeletal muscle, heart, and kidney, and it is shown to implicate in many diseases, such as multiple sclerosis (MS), Guillain-Barre syndrome (GBS), Alexander disease, epilepsy, Down syndrome, familial amyotrophic lateral sclerosis (FALS), familial amyloidotic polyneuropathy and chronic inflammatory demyelinating polyneuropathy [1–8]. It has been reported that α-BC functions as molecular chaperones by binding with denatured protein under stress in a reversible equilibrium state. In addition, the specific interaction between α-BC and cytoskeletal structures in cardiac and skeletal myocytes has been proved, and the interaction is enhanced after stress, which contributes to increased stress tolerance [9–12]. The increased expression of α-BC in cerebral arteriovenous malformations (AVMs) is also associated with maintenance of the intermediate fibre (IF) network, which increases wall tension caused by dilating vessels and the hemodynamic stress surrounding [13], another research found out that α-BC significantly suppressed the ADP-induced secretions of both platelet-derived growth factor (PDGF) and serotonin by inhibition of HSP27 phosphorylation via p44/p42
Analysis of the NMDA in Focal Cerebral Ischemia in Rats
Tirapelli,D. P. C; Carlotti Jr,C. G; Leite,J. P; Lizarte,F. S. N; Tirapelli,L. F; Colli,B. O;
International Journal of Morphology , 2012, DOI: 10.4067/S0717-95022012000300035
Abstract: nmdar (n-methyl-d-aspartate receptor) is one subtype of ionotrophic glutamate receptor which is extensively distributed in the central nervous system (cns). in the mammalian cns, nmdar serves prominent roles in the pathophysiologic process of cerebral ischemia. this study aimed to investigate the pattern of expression of protein and gene of the excitatory neurotransmitter nmdar in experimental focal cerebral ischemia and the hole of neuroprotection with hypothermia and ketoprofen. 120 rats were randomly divided into 6 groups (20 animals each): control - no surgery; sham - simulation of surgery; ischemic - focal ischemia for 1 hour, without reperfusion; ischemic + intraischemic hypothermia; ischemic + previous intravenous ketoprofen, and ischemic + hypothermia and ketoprofen. ten animals from each experimental group were used to establish the volume of infarct. transient focal cerebral ischemia was obtained in rats by occlusion of the middle cerebral artery with an intraluminal suture. the infarct volume was measured using morphometric analysis of infarct areas defined by triphenyl tetrazolium chloride and the patterns of expression of the protein and gene nmda were evaluated by immunohistochemistry and quantitative real-time pcr, respectively. increases in the protein and gene nmda receptor in the ischemics areas were observed and these increases were reduced by hypothermia and ketoprofen. the increase in the nmda receptor protein and gene expression observed in the ischemic animals was reduced by neuroprotection (hypothermia and ketoprofen). the nmda receptor increases in the ischemic area suggests that the nmda mediated neuroexcitotoxicity plays an important role in cell death and that the neuroprotective effect of both, hypothermia and ketoprofen is directly involved with the nmda.
Synthesis and Protective Effect of Scutellarein on Focal Cerebral Ischemia/Reperfusion in Rats  [PDF]
Lihua Qian,Minzhe Shen,Hao Tang,Yuping Tang,Li Zhang,Yifan Fu,Qianping Shi,Nian-Guang Li
Molecules , 2012, DOI: 10.3390/molecules170910667
Abstract: Scutellarein, the main metabolite of scutellarin in vivo, has relatively better solubility, bioavailability and bio-activity than scutellarin. However, compared with scutellarin, it is very difficult to obtain scutellarein from Nature. Therefore, the present study focused on establishing an efficient route for the synthesis of scutellarein by hydrolyzing scutellarin. Neurological deficit score and cerebral infarction volume with the administration of scutellarein were then used to compare its neuroprotective effects on focal cerebral ischemia/reperfusion in rats induced by middle cerebral artery occlusion (MCAO) with those of scutellarin. The results showed that scutellarein had better protective effect on focal cerebral ischemia/reperfusion than scutellarin, which laid the foundation for further research and development of scutellarein as a promising candidate for ischemic cerebro-vascular disease.
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