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Jaroslaw Aronowski - One of the best experts on this subject based on the ideXlab platform.
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neuronal expression of peroxisome proliferator activated receptor gamma pparγ and 15d prostaglandin j2 mediated protection of brain after experimental cerebral Ischemia in rat
Brain Research, 2006Co-Authors: Xiurong Zhao, Lise A Labiche, Roger Strong, James C Grotta, Oliver Herrmann, Jaroslaw AronowskiAbstract:Abstract Existing experimental evidence suggests that PPARγ may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral Ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARγ messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARγ mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARγ in neurons after Ischemia. Intraventricular injection of 15d-Δ12,14-prostaglandin J2 (15d-PGJ2), a proposed endogenous PPARγ agonist, into the ischemic rat brains significantly increased the PPARγ-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARγ up-regulation in response to Ischemia may contribute to PPARγ activation in the presence of PPARγ agonists. Activation of PPARγ in neurons at an early stage after Ischemia may represent a pro-survival mechanism against ischemic injury.
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Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2—Mediated protection of brain after experimental cerebral Ischemia in rat
Brain Research, 2006Co-Authors: Xiurong Zhao, Lise A Labiche, Roger Strong, James C Grotta, Oliver Herrmann, Jaroslaw AronowskiAbstract:Abstract Existing experimental evidence suggests that PPARγ may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral Ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARγ messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARγ mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARγ in neurons after Ischemia. Intraventricular injection of 15d-Δ12,14-prostaglandin J2 (15d-PGJ2), a proposed endogenous PPARγ agonist, into the ischemic rat brains significantly increased the PPARγ-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARγ up-regulation in response to Ischemia may contribute to PPARγ activation in the presence of PPARγ agonists. Activation of PPARγ in neurons at an early stage after Ischemia may represent a pro-survival mechanism against ischemic injury.
Heng Zhao - One of the best experts on this subject based on the ideXlab platform.
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ischemic tolerance in situ and remote pre and postconditioning
Primer on Cerebrovascular Diseases, 2017Co-Authors: Heng ZhaoAbstract:Abstract Ischemic tolerance was originally induced by in situ ischemic preconditioning (PreC, i.e., before Ischemia). This classic concept of ischemic PreC has now evolved into ischemic postconditioning (PostC, i.e., after Ischemia), remote PreC and PostC, and remote perconditioning (PerC, i.e., during Ischemia). In addition, ischemic tolerance induced by ischemic PreC and PostC can be triggered by many nonischemic stressors. Each type of ischemic conditioning has specific therapeutic time windows, and unique protective mechanisms. PreC adapts the brain to resist brain injury induced by a subsequent severe stroke; PostC alters reperfusion after a stroke to attenuate the brain injury it caused. In contrast, remote conditioning exerts its effect on the brain via various factors produced in the remote ischemic organ. Despite these differences, the protective mechanisms of in situ and remote conditioning converge on some similar cellular and molecular mechanisms at a later stage after stroke.
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Abstract TP259: Ischemic Postconditioning Protects Against Focal Ischemia in Mouse
Stroke, 2013Co-Authors: Sungpil Joo, Weiying Xie, Heng ZhaoAbstract:Ischemic Postconditioning Protects Against Focal Ischemia in Mouse Background: Ischemic postconditioning(IPost) has been shown to attenuate cerebral Ischemia/reperfusion injury in a few rat models....
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The Protective Effects of Ischemic Postconditioning in Experimental Stroke
Innate Tolerance in the CNS, 2012Co-Authors: Heng ZhaoAbstract:In contrast to ischemic preconditioning, which is sublethal Ischemia and reperfusion performed before stroke onset to mitigate its effects, ischemic postconditioning refers to the protective effects of reperfusion interruption performed after the restoration of blood flow following stroke. This chapter focuses on the protective effects of ischemic postconditioning in various ischemic models, including in vivo focal and global Ischemia models as well as in vitro oxygen glucose deprivation (OGD) models. Different triggers used to mimic the effects of ischemic postconditioning are discussed, including brief, repetitive reperfusion/occlusion of blood vessels, a single period of brief Ischemia or hypoxia, and application of neurotoxic or anesthetic agents. In addition, the chronic protective effects of ischemic postconditioning and the therapeutic time windows are summarized. Furthermore, the potential for a combination of ischemic pre- and postconditioning to generate synergistic effects is explored. Last, the underlying protective mechanisms of postconditioning, such as the Akt cell survival pathway, MAPK pathways, and PKC pathways, among others, are discussed. This chapter therefore offers a comprehensive review on the progress of research in ischemic postconditioning for stroke.
Shinichi Takamoto - One of the best experts on this subject based on the ideXlab platform.
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Long-term treatment with nipradilol, a nitric oxide–releasing β-adrenergic blocker, enhances postischemic recovery and limits infarct size
The Annals of thoracic surgery, 2002Co-Authors: Yoshihiro Suematsu, Toshiya Ohtsuka, Hitoshi Horimoto, Katsuhide Maeda, Yasunari Nakai, Shigetoshi Mieno, Shinichi TakamotoAbstract:Abstract Background . This study examines whether the chronic administration of nipradilol, a nitric oxide–releasing β-adrenergic blocker, decreases Ischemia-reperfusion injury. Methods . Rats were treated with nipradilol (10 mg/kg per day orally) or a vehicle alone for 4 weeks. Isolated rat hearts were assigned to one of five groups (each n=6): global Ischemia groups treated with the vehicle or with nipradilol were subjected to 20 minutes of Ischemia; ischemic preconditioning groups treated with the vehicle or with nipradilol were subjected to 3 minutes of ischemic preconditioning; and the l-arginine group treated with the vehicle received 1 mmol/L of l-arginine before global Ischemia. Hemodynamic variables and coronary flow were recorded continuously. Nitrites and nitrates levels were measured 60 minutes after reperfusion, and the infarct size was determined. In another series (each n=6), lipid peroxidation was investigated. Results . In the nipradilol group, significant preservation of the left ventricular pressure and coronary flow, as well as the level of nitrates and nitrites, was observed, compared with the global Ischemia group. The infarct size was also significantly reduced in the ischemic preconditioning (23.5% ± 5.47%), l-arginine (25.6% ± 5.59%), and especially the nipradilol (10.7% ± 1.65%) groups. However, in the nipradilol plus ischemic preconditioning group, the protective effects were eliminated. Lipid peroxidation after nipradilol treatment was significantly reduced before and after global Ischemia, compared with the global Ischemia group. Conclusions . The chronic administration of nipradilol improves postischemic functional recovery and infarct size, partly by preventing the formation of lipid peroxides. These cardioprotective effects were, however, abolished by ischemic preconditioning.
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long term treatment with nipradilol a nitric oxide releasing β adrenergic blocker enhances postischemic recovery and limits infarct size
The Annals of Thoracic Surgery, 2002Co-Authors: Yoshihiro Suematsu, Toshiya Ohtsuka, Hitoshi Horimoto, Katsuhide Maeda, Yasunari Nakai, Shigetoshi Mieno, Shinichi TakamotoAbstract:Abstract Background . This study examines whether the chronic administration of nipradilol, a nitric oxide–releasing β-adrenergic blocker, decreases Ischemia-reperfusion injury. Methods . Rats were treated with nipradilol (10 mg/kg per day orally) or a vehicle alone for 4 weeks. Isolated rat hearts were assigned to one of five groups (each n=6): global Ischemia groups treated with the vehicle or with nipradilol were subjected to 20 minutes of Ischemia; ischemic preconditioning groups treated with the vehicle or with nipradilol were subjected to 3 minutes of ischemic preconditioning; and the l-arginine group treated with the vehicle received 1 mmol/L of l-arginine before global Ischemia. Hemodynamic variables and coronary flow were recorded continuously. Nitrites and nitrates levels were measured 60 minutes after reperfusion, and the infarct size was determined. In another series (each n=6), lipid peroxidation was investigated. Results . In the nipradilol group, significant preservation of the left ventricular pressure and coronary flow, as well as the level of nitrates and nitrites, was observed, compared with the global Ischemia group. The infarct size was also significantly reduced in the ischemic preconditioning (23.5% ± 5.47%), l-arginine (25.6% ± 5.59%), and especially the nipradilol (10.7% ± 1.65%) groups. However, in the nipradilol plus ischemic preconditioning group, the protective effects were eliminated. Lipid peroxidation after nipradilol treatment was significantly reduced before and after global Ischemia, compared with the global Ischemia group. Conclusions . The chronic administration of nipradilol improves postischemic functional recovery and infarct size, partly by preventing the formation of lipid peroxides. These cardioprotective effects were, however, abolished by ischemic preconditioning.
Xiurong Zhao - One of the best experts on this subject based on the ideXlab platform.
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neuronal expression of peroxisome proliferator activated receptor gamma pparγ and 15d prostaglandin j2 mediated protection of brain after experimental cerebral Ischemia in rat
Brain Research, 2006Co-Authors: Xiurong Zhao, Lise A Labiche, Roger Strong, James C Grotta, Oliver Herrmann, Jaroslaw AronowskiAbstract:Abstract Existing experimental evidence suggests that PPARγ may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral Ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARγ messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARγ mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARγ in neurons after Ischemia. Intraventricular injection of 15d-Δ12,14-prostaglandin J2 (15d-PGJ2), a proposed endogenous PPARγ agonist, into the ischemic rat brains significantly increased the PPARγ-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARγ up-regulation in response to Ischemia may contribute to PPARγ activation in the presence of PPARγ agonists. Activation of PPARγ in neurons at an early stage after Ischemia may represent a pro-survival mechanism against ischemic injury.
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Neuronal expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and 15d-prostaglandin J2—Mediated protection of brain after experimental cerebral Ischemia in rat
Brain Research, 2006Co-Authors: Xiurong Zhao, Lise A Labiche, Roger Strong, James C Grotta, Oliver Herrmann, Jaroslaw AronowskiAbstract:Abstract Existing experimental evidence suggests that PPARγ may play a beneficial role in neuroprotection from various brain pathologies. Here we found that focal cerebral Ischemia induced by middle cerebral/common carotid arteries occlusion (MCA/CCAo) induced up-regulation of PPARγ messenger RNA in the ischemic hemisphere as early as 6 h after the ischemic event. The increased PPARγ mRNA expression was primarily associated with neurons in the ischemic penumbra, suggesting an important role for PPARγ in neurons after Ischemia. Intraventricular injection of 15d-Δ12,14-prostaglandin J2 (15d-PGJ2), a proposed endogenous PPARγ agonist, into the ischemic rat brains significantly increased the PPARγ-DNA-binding activity and reduced infarction volume at 24 h after reperfusion. We propose that PPARγ up-regulation in response to Ischemia may contribute to PPARγ activation in the presence of PPARγ agonists. Activation of PPARγ in neurons at an early stage after Ischemia may represent a pro-survival mechanism against ischemic injury.
Yoshihiro Suematsu - One of the best experts on this subject based on the ideXlab platform.
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Long-term treatment with nipradilol, a nitric oxide–releasing β-adrenergic blocker, enhances postischemic recovery and limits infarct size
The Annals of thoracic surgery, 2002Co-Authors: Yoshihiro Suematsu, Toshiya Ohtsuka, Hitoshi Horimoto, Katsuhide Maeda, Yasunari Nakai, Shigetoshi Mieno, Shinichi TakamotoAbstract:Abstract Background . This study examines whether the chronic administration of nipradilol, a nitric oxide–releasing β-adrenergic blocker, decreases Ischemia-reperfusion injury. Methods . Rats were treated with nipradilol (10 mg/kg per day orally) or a vehicle alone for 4 weeks. Isolated rat hearts were assigned to one of five groups (each n=6): global Ischemia groups treated with the vehicle or with nipradilol were subjected to 20 minutes of Ischemia; ischemic preconditioning groups treated with the vehicle or with nipradilol were subjected to 3 minutes of ischemic preconditioning; and the l-arginine group treated with the vehicle received 1 mmol/L of l-arginine before global Ischemia. Hemodynamic variables and coronary flow were recorded continuously. Nitrites and nitrates levels were measured 60 minutes after reperfusion, and the infarct size was determined. In another series (each n=6), lipid peroxidation was investigated. Results . In the nipradilol group, significant preservation of the left ventricular pressure and coronary flow, as well as the level of nitrates and nitrites, was observed, compared with the global Ischemia group. The infarct size was also significantly reduced in the ischemic preconditioning (23.5% ± 5.47%), l-arginine (25.6% ± 5.59%), and especially the nipradilol (10.7% ± 1.65%) groups. However, in the nipradilol plus ischemic preconditioning group, the protective effects were eliminated. Lipid peroxidation after nipradilol treatment was significantly reduced before and after global Ischemia, compared with the global Ischemia group. Conclusions . The chronic administration of nipradilol improves postischemic functional recovery and infarct size, partly by preventing the formation of lipid peroxides. These cardioprotective effects were, however, abolished by ischemic preconditioning.
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long term treatment with nipradilol a nitric oxide releasing β adrenergic blocker enhances postischemic recovery and limits infarct size
The Annals of Thoracic Surgery, 2002Co-Authors: Yoshihiro Suematsu, Toshiya Ohtsuka, Hitoshi Horimoto, Katsuhide Maeda, Yasunari Nakai, Shigetoshi Mieno, Shinichi TakamotoAbstract:Abstract Background . This study examines whether the chronic administration of nipradilol, a nitric oxide–releasing β-adrenergic blocker, decreases Ischemia-reperfusion injury. Methods . Rats were treated with nipradilol (10 mg/kg per day orally) or a vehicle alone for 4 weeks. Isolated rat hearts were assigned to one of five groups (each n=6): global Ischemia groups treated with the vehicle or with nipradilol were subjected to 20 minutes of Ischemia; ischemic preconditioning groups treated with the vehicle or with nipradilol were subjected to 3 minutes of ischemic preconditioning; and the l-arginine group treated with the vehicle received 1 mmol/L of l-arginine before global Ischemia. Hemodynamic variables and coronary flow were recorded continuously. Nitrites and nitrates levels were measured 60 minutes after reperfusion, and the infarct size was determined. In another series (each n=6), lipid peroxidation was investigated. Results . In the nipradilol group, significant preservation of the left ventricular pressure and coronary flow, as well as the level of nitrates and nitrites, was observed, compared with the global Ischemia group. The infarct size was also significantly reduced in the ischemic preconditioning (23.5% ± 5.47%), l-arginine (25.6% ± 5.59%), and especially the nipradilol (10.7% ± 1.65%) groups. However, in the nipradilol plus ischemic preconditioning group, the protective effects were eliminated. Lipid peroxidation after nipradilol treatment was significantly reduced before and after global Ischemia, compared with the global Ischemia group. Conclusions . The chronic administration of nipradilol improves postischemic functional recovery and infarct size, partly by preventing the formation of lipid peroxides. These cardioprotective effects were, however, abolished by ischemic preconditioning.
