Therapeutic window for cinnamophilin following oxygen–glucose deprivation and transient focal cerebral ischemia

Lee, E-Jian; Chen, Hung-Yi; Hung, Yao-Min; Chen, Tsung-Ying; Lee, Ming-Yang; Yu, Shu-Ching; Chen, Ying-Hsin; Chuang, I-Chuan; Wu, Tong

doi:10.1016/j.expneurol.2009.01.019

Cited by 40 publications

(61 citation statements)

References 42 publications

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“…Generally, longer therapeutic windows are described in studies using mice in which tMCAO is of brief duration (≤30 minutes), 26,27 whereas most studies in rats used a 90-to 120-minute tMCAO. 7,[28][29][30][31] A study using NA-1 in primates suggests efficacy in a 3.5-hour tMCAO when the treatment was administered 3 hours after ischemia onset. 9 However, this study, conducted in our laboratory, was in a tMCAO model in which a collateral circulation was purposely maintained to preserve a penumbra by 3 hours.…”

Section: Strokementioning

confidence: 99%

Novel Approaches to Neuroprotection Trials in Acute Ischemic Stroke

Tymianski

2013

Stroke

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Section: Strokementioning

confidence: 99%

Novel Approaches to Neuroprotection Trials in Acute Ischemic Stroke

Tymianski

2013

Stroke

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“…Our previous works have also demonstrated that CINN effectively scavenged free radicals and improved the endogenous antioxidant defense to the tissues at risk of brain infarction. Additionally, CINN had antioxidant effects by reducing the malondialdehyde levels in the ischemic brain tissues and the Fe 3+ -induced lipid peroxidation in rat brain homogenate [26]. Thus, treatment with CINN could result in a marked reduction in postischemic accumulations of ROS and, consequently, attenuated the extent of lipid peroxidation, oxidative the PMA-stimulated neutrophils ( Figure 6B, P<0.05).…”

Section: Discussionmentioning

confidence: 85%

“…We have previously demonstrated that CINN not only reduced brain infarction and oxidative stress, but also improved behavioral outcome in a mouse model of transient middle cerebral artery (MCA) occlusion [26,27]. More recently, we have demonstrated that CINN exhibited anti-inflammatory actions against ischemic stroke [26].…”

Section: Introductionmentioning

confidence: 99%

Cinnamophilin Inhibits Neutrophilic Respiratory Burst and Protects Against Ischemia-Reperfusion Brain Damage

Tien¹

2013

Pharm Anal Acta

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“…During surgery, body temperature was maintained at 37.0 AE 0.58C using a thermostatically controlled heating blanket and rectal probe (Harvard Apparatus, South Natick, MA). Focal cerebral ischemia was employed by intraarterial suture occlusion of the proximal right MCA by the method described previously (8)(9)(10)(11). Briefly, bifurcation of the right common carotid artery was exposed under an operating microscope.…”

Section: Transient Middle Cerebral Artery (Mca) Occlusionmentioning

confidence: 99%

“…The calculated infarction areas on the 12 predetermined coronal sections were then compiled to obtain infarct volume (in mm 3 ). Infarct volumes were expressed as a percentage of the contralateral hemisphere volume by using an ''indirect method'' (8)(9)(10)(11).…”

Section: Histologymentioning

confidence: 99%

Optimal Percoll concentration facilitates flow cytometric analysis for annexin V/propidium iodine‐stained ischemic brain tissues

et al. 2012

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We sought to determine the optimal Percoll concentration for ischemic rat brain prepared for flow cytometric (FC) measurements. Animals were subjected to the right middle cerebral artery (MCA) occlusion, and were euthanized at 3, 12, 24, and 72 h after reperfusion onset. The brains were processed by different concentrations (unisolated, 20, 25, 30, or 40%) of Percoll and stained with annexin V/propidium iodine (PI). Ischemic brain damage was evaluated by FC analysis and image analysis for histologic sections. The relative susceptibility of different phenotypes of cells to necrotic and apoptotic damage were evaluated by the FC analyses for the immunohistochemistry, PI, and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-processed brain tissues. Our results showed that FC analysis effectively detected the extent and maturation of apoptotic/necrotic brain damage, and the results were consistent with those determined from histologic brain sections. Neuron was more vulnerable to apoptosis than glia, whereas both cellular phenotypes were compatible in susceptibility for necrotic cell death. Percoll at a low concentration (20%) could effectively remove tissue debris without affecting membranous integrity of the injured neurons. Conversely, high percentages of Percoll (30-40%) substantially increased membranous damage for the injured cells. These results supported the application of FC to determine the extent and progression in time, as well as relative phenotypes of apoptotic/necrotic cell deaths following ischemic damage. We highlighted the use of Percoll at low percentages to facilitate the removal of tissue debris and to improve membrane integrity preservation for the injured neurons. ' 2012 International Society for Advancement of CytometryKey terms stroke; apoptosis; necrosis; phosphatidyl serine; flow cytometry BRAIN ischemia induces numerous deleterious cascades such as ionic imbalance, receptor activation, and excessive production of excitatory amino acids and free radicals, each of which may lead to cellular necrotic, apoptotic, or even autophagy injury. Necrosis results when the integrity of cytoplasmic membranes become compromised, and, thus, the event can easily be detected by staining with propidium iodine (PI). In contrast, apoptotic cells are characterized by loss of membranes phospholipid symmetry and exposure of phosphatidyl serine (PS) at the cell surface, followed by condensed chromatin structure, reduced cell volume and DNA fragmentations (1,2). Annexin V and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) techniques, which selectively binds to negatively charged phospholipids and 3 0 -hydroxyl terminal of DNA strand breaks, respectively, are therefore, widely used to identify apoptotic cell injury (3,4).Histologic assessment in experimental stroke is largely dominated by the use of traditional brain section staining for the damage to neuronal perikarya and labeling

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Therapeutic window for cinnamophilin following oxygen–glucose deprivation and transient focal cerebral ischemia

Cited by 40 publications

References 42 publications

Novel Approaches to Neuroprotection Trials in Acute Ischemic Stroke

Novel Approaches to Neuroprotection Trials in Acute Ischemic Stroke

Cinnamophilin Inhibits Neutrophilic Respiratory Burst and Protects Against Ischemia-Reperfusion Brain Damage

Optimal Percoll concentration facilitates flow cytometric analysis for annexin V/propidium iodine‐stained ischemic brain tissues

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