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JCI:葡萄糖引起低血糖昏迷的大鼠脑细胞死亡

来源:华文生技网 2007-04-18 09:15

    根据一项由旧金山VA 医疗中心的研究人员利用啮齿目动物进行的研究显示,一般认为由于低血糖导致的昏迷,实际上是在给予葡萄糖时发生的损伤。

    胰岛素是使葡萄糖从血液移动至细胞的重要激素。糖尿病患者无法制造足够的胰岛素,必须一天注射多次胰岛素。

    严重的胰岛素药剂过量,可能使血液中的葡萄糖含量降低至过低的程度,这种情况又称为低血糖症,并且会造成低血糖昏迷,造成神经元受到破坏。

    而这项研究第一次让研究人员知道,大鼠的脑损伤并非发生于低血糖昏迷期间,而是在给予葡萄糖且血液葡萄糖含量恢复正常之后。研究人员也辨认出造成脑损伤的起因:葡萄糖突然回到脑部,会活化酵素NADPH 氧化酶,并引起氧化压力而造成神经元死亡。

    这项研究结果是令人惊讶的,而且对于糖尿病患者的低血糖昏迷之治疗,有很大的影响。

     (资料来源 : Bio.com)

原始出处:

http://www.bio.com/newsfeatures/newsfeatures_research.jhtml;jsessionid=BAKFVNQJPDRIXR3FQLMSFEWHUWBNQIV0?cid=28100007

 

部分英文原文:

J. Clin. Invest. 117:910-918 (2007). doi:10.1172/JCI30077.

Research Article

Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase

Sang Won Suh1, Elizabeth T. Gum1, Aaron M. Hamby1, Pak H. Chan2 and Raymond A. Swanson1

1Department of Neurology, UCSF, and Veterans Affairs Medical Center, San Francisco, California, USA. 2Department of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, California, USA.

Address correspondence to: Raymond A. Swanson, (127) Neurology, Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, California 94121, USA. Phone: (415) 750-2011; Fax: (415) 750-2273; E-mail: raymond.swanson@ucsf.edu .

Received for publication August 16, 2006, and accepted in revised form January 30, 2007.

Abstract

Hypoglycemic coma and brain injury are potential complications of insulin therapy. Certain neurons in the hippocampus and cerebral cortex are uniquely vulnerable to hypoglycemic cell death, and oxidative stress is a key event in this cell death process. Here we show that hypoglycemia-induced oxidative stress and neuronal death are attributable primarily to the activation of neuronal NADPH oxidase during glucose reperfusion. Superoxide production and neuronal death were blocked by the NADPH oxidase inhibitor apocynin in both cell culture and in vivo models of insulin-induced hypoglycemia. Superoxide production and neuronal death were also blocked in studies using mice or cultured neurons deficient in the p47phox subunit of NADPH oxidase. Chelation of zinc with calcium disodium EDTA blocked both the assembly of the neuronal NADPH oxidase complex and superoxide production. Inhibition of the hexose monophosphate shunt, which utilizes glucose to regenerate NADPH, also prevented superoxide formation and neuronal death, suggesting a mechanism linking glucose reperfusion to superoxide formation. Moreover, the degree of superoxide production and neuronal death increased with increasing glucose concentrations during the reperfusion period. These results suggest that high blood glucose concentrations following hypoglycemic coma can initiate neuronal death by a mechanism involving extracellular zinc release and activation of neuronal NADPH oxidase.

英文全文链接http://www.jci.org/cgi/content/full/117/4/910

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