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【文摘发布】来普汀(一种减肥药)对氧-糖剥夺

Title:Neuroprotective Effects of Leptin Against Ischemic Injury Induced by Oxygen-Glucose Deprivation and Transient Cerebral Ischemia.

Author:Zhang F, Wang S, Signore AP, Chen J.
From the Departments of Neurology and Pharmacology, University of Pittsburgh, and the Geriatric Research, Educational and Clinical Center, VA Pittsburgh Health Care System, Pittsburgh, Pa.

Resource: Stroke. 2007 Jun 28; [Epub ahead of print]

Abstract:BACKGROUND AND PURPOSE: Leptin is the major adipose hormone that regulates body weight and energy expenditure by activating leptin receptors in the hypothalamus. Leptin receptors are also present in other cell types, and a potent antiapoptotic effect for leptin has recently been reported. We investigated whether leptin was neuroprotective against ischemic brain injury. METHODS: In vitro ischemic injury was induced in rat primary neuronal culture by oxygen-glucose deprivation for 90 minutes. In vivo ischemic brain injury was induced by middle cerebral artery occlusion in mice for 60 minutes. RESULTS: Leptin receptors were detected in cultured rat cortical neurons, as well as in the mouse cortex, striatum, and hippocampus. In vitro results showed that leptin, 50 to 100 microg/mL, protected primary cortical neurons against death induced by oxygen-glucose deprivation in a concentration-dependent manner. In vivo studies in the mouse brain demonstrated that the intraperitoneal administration of leptin, 2 to 8 mg/kg, dose-dependently reduced infarct volume induced by middle cerebral artery occlusion. Leptin was effective when injected 5 minutes before or 30 to 90 minutes after reperfusion, but not 2 hours after reperfusion. Leptin improved animal body weight recovery and behavioral parameters after cerebral ischemia. Leptin enhanced the phosphorylation of extracellular signal-related kinase 1/2. Both extracellular signal-related kinase 1/2 activation and neuroprotection were abolished by the administration of PD98059 in vitro and in vivo. CONCLUSIONS: Leptin is neuroprotective against ischemic neuronal injury. Our findings suggest that leptin is a legitimate candidate for the treatment of ischemic stroke.

PMID: 17600230

国人写的文章,支持一下! 本人已认领该文编译,48小时后若未提交译文,请其他战友自由认领。 Leptin瘦素,是由肥胖基因(ob基因)在脂肪组织特异性表达、合成和分泌的蛋白激素,它控制摄食和能量代谢,是调节肥胖的一个重要因素. Title:Neuroprotective Effects of Leptin Against Ischemic Injury Induced by Oxygen-Glucose Deprivation and Transient Cerebral Ischemia.
标题:来普汀(瘦素)对缺氧缺糖和短暂性脑缺血所诱发的局部缺血性损害的神经保护作用
Author:Zhang F, Wang S, Signore AP, Chen J.
作者:Zhang F, Wang S, Signore AP, Chen J
From the Departments of Neurology and Pharmacology, University of Pittsburgh, and the Geriatric Research, Educational and Clinical Center, VA Pittsburgh Health Care System, Pittsburgh, Pa.
来自匹兹堡大学神经学和药理学系及宾州匹兹堡退伍军人管理局匹兹堡卫生保健系统老年病学研究教育与临床中心。

Resource: Stroke. 2007 Jun 28; [Epub ahead of print]
文章来源:《卒中》杂志2007 年6 月28;
Abstract:BACKGROUND AND PURPOSE: Leptin is the major adipose hormone that regulates body weight and energy expenditure by activating leptin receptors in the hypothalamus.
摘要:
背景和目的:
来普汀是一种通过激活下丘脑的来普汀受体来调节体重及能量消耗的重要脂质激素。
Leptin receptors are also present in other cell types, and a potent antiapoptotic effect for leptin has recently been reported. We investigated whether leptin was neuroprotective against ischemic brain injury.
来普汀受体也出现在其他类型细胞中,并且最近报告了来普汀潜在的抗细胞凋亡作用。我们对来普汀是否对局部缺血性脑损伤有神经保护作用进行了研究。
METHODS: In vitro ischemic injury was induced in rat primary neuronal culture by oxygen-glucose deprivation for 90 minutes. In vivo ischemic brain injury was induced by middle cerebral artery occlusion in mice for 60 minutes.
方法:
通过使培养的大鼠原代神经细胞缺氧缺糖90分钟造成体外局部缺血损伤模型。通过闭塞小鼠大脑中动脉60分钟造成体内局部缺血脑损伤模型。
RESULTS: Leptin receptors were detected in cultured rat cortical neurons, as well as in the mouse cortex, striatum, and hippocampus.
结果:
除了在小鼠脑皮层、纹状体和海马体中发现普汀受体外,在培养的大鼠皮质神经元中也发现来普汀受体。
In vitro results showed that leptin, 50 to 100 microg/mL, protected primary cortical neurons against death induced by oxygen-glucose deprivation in a concentration-dependent manner. In vivo studies in the mouse brain demonstrated that the intraperitoneal administration of leptin, 2 to 8 mg/kg, dose-dependently reduced infarct volume induced by middle cerebral artery occlusion.

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作者:admin@医学,生命科学    2011-02-14 18:19
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