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血管生成素样蛋白1可减轻小鼠局灶性脑缺血后的血脑屏障损伤和水肿。

Angiopoietin-like protein 1 decreases blood brain barrier damage and edema following focal cerebral ischemia in mice.

作者信息

Lai Dar-Ming, Li Hung, Lee Chin-Cheng, Tzeng Yi-Shiuan, Hsieh Yu-Hsuan, Hsu Wen-Ming, Hsieh Fon-Jou, Cheng Juei-Tang, Tu Yong-Kwang

机构信息

Division of Neurosurgery, Department of Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.

出版信息

Neurochem Int. 2008 Feb;52(3):470-7. doi: 10.1016/j.neuint.2007.08.010. Epub 2007 Aug 22.

Abstract

Angiopoietin-like protein (Angptl) 1, a member of the angiopoietin-related protein family, modulates angiogenesis but little else is known of its physiological role. We found that angptl1 was upregulated at the 7th day after focal cerebral ischemia in normal mice. In order to understand the role of angptl1 in cerebral infarction, we induced focal cerebral ischemia in normal and glial fibrillary acidic protein promoter-angptl1 transgenic mice. In the transgenic mice without ischemia, overexpression of angptl1 in the whole brain led to a decrease in cortical microvascular density. Following focal cerebral ischemia, edema, but not infarct size, was less in transgenic mice relative to wild type littermates. This effect might be due to a reduction in the blood brain barrier breakdown, as confirmed by a decrease in Evans Blue leakage in the early post-ischemic phase. We conclude that angptl1 may have a beneficial role in the preservation of vascular integrity following focal cerebral ischemia.

摘要

血管生成素样蛋白(Angptl)1是血管生成素相关蛋白家族的成员之一,可调节血管生成,但对其生理作用了解甚少。我们发现,正常小鼠局灶性脑缺血后第7天,angptl1表达上调。为了了解angptl1在脑梗死中的作用,我们在正常小鼠和胶质纤维酸性蛋白启动子-angptl1转基因小鼠中诱导局灶性脑缺血。在未发生缺血的转基因小鼠中,全脑angptl1过表达导致皮质微血管密度降低。局灶性脑缺血后,转基因小鼠的水肿(而非梗死面积)相对于野生型同窝小鼠较轻。这种作用可能是由于血脑屏障破坏减少所致,缺血后早期伊文思蓝渗漏减少证实了这一点。我们得出结论,angptl1在局灶性脑缺血后保护血管完整性方面可能具有有益作用。

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