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胰岛素神经保护作用及其机制。

Insulin neuroprotection and the mechanisms.

作者信息

Yu Li-Yun, Pei Yu

机构信息

Department of Endocrinology, Chinese PLA General Hospital, Beijing 100853, China.

出版信息

Chin Med J (Engl). 2015 Apr 5;128(7):976-81. doi: 10.4103/0366-6999.154323.

DOI:10.4103/0366-6999.154323
PMID:25836621
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4834017/
Abstract

OBJECTIVE

To analyze the mechanism of neuroprotection of insulin and which blood glucose range was benefit for insulin exerting neuroprotective action.

DATA SOURCES

The study is based on the data from PubMed.

STUDY SELECTION

Articles were selected with the search terms "insulin", "blood glucose", "neuroprotection", "brain", "glycogen", "cerebral ischemia", "neuronal necrosis", "glutamate", "γ-aminobutyric acid".

RESULTS

Insulin has neuroprotection. The mechanisms include the regulation of neurotransmitter, promoting glycogen synthesis, and inhibition of neuronal necrosis and apoptosis. Insulin could play its role in neuroprotection by avoiding hypoglycemia and hyperglycemia.

CONCLUSIONS

Intermittent and long-term infusion insulin may be a benefit for patients with ischemic brain damage at blood glucose 6-9 mmol/L.

摘要

目的

分析胰岛素的神经保护机制以及哪个血糖范围有利于胰岛素发挥神经保护作用。

资料来源

本研究基于来自PubMed的数据。

研究选择

通过检索词“胰岛素”“血糖”“神经保护”“脑”“糖原”“脑缺血”“神经元坏死”“谷氨酸”“γ-氨基丁酸”选择文章。

结果

胰岛素具有神经保护作用。其机制包括调节神经递质、促进糖原合成以及抑制神经元坏死和凋亡。胰岛素可通过避免低血糖和高血糖发挥其神经保护作用。

结论

对于血糖在6 - 9 mmol/L的缺血性脑损伤患者,间歇性和长期输注胰岛素可能有益。

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本文引用的文献

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Activation of hepatic inflammatory pathways by catecholamines is associated with hepatic insulin resistance in male ischemic stroke rats.儿茶酚胺激活肝炎症途径与雄性缺血性脑卒中大鼠肝胰岛素抵抗有关。
Endocrinology. 2014 Apr;155(4):1235-46. doi: 10.1210/en.2013-1593. Epub 2014 Jan 17.
2
Cytochrome C is tyrosine 97 phosphorylated by neuroprotective insulin treatment.细胞色素 C 是由神经保护作用的胰岛素治疗所磷酸化的酪氨酸 97。
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Insulin promotes glycogen storage and cell proliferation in primary human astrocytes.胰岛素促进原代人星形胶质细胞的糖原储存和细胞增殖。
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Insulin and glucagon share the same mechanism of neuroprotection in diabetic rats: role of glutamate.胰岛素和胰高血糖素在糖尿病大鼠中具有相同的神经保护机制:谷氨酸的作用。
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Cleavage of the vesicular GABA transporter under excitotoxic conditions is followed by accumulation of the truncated transporter in nonsynaptic sites.在兴奋性毒性条件下,囊泡 GABA 转运体被切割,随后截短的转运体在非突触部位积累。
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