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首页> 外文期刊>Life sciences >Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats
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Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats

机译：胰岛素恢复链脲佐菌素诱导的糖尿病大鼠神经元一氧化氮合酶表达

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摘要

Nitric oxide (NO) is known to play an important role in the pathophysiology of insulin-dependent diabetic mellitus (IDDM). In an attempt to investigate the relation between insulin and NO in IDDM, the present study employed male Wistar rats to induce IDDM by intravenous injection of streptozotocin (STZ). Four groups of rats were used; untreated normal control group, insulin treated STZ group, vehicle-treated STZ control, and one group of age-matched rats which were orally supplied with glucose to increase plasma glucose (glucose-challenged rats). Changes of the activity and gene expression of neuronal nitric oxide synthase (nNOS) were examined in cerebellum and kidney of these groups. The activity of nNOS in cerebellum, determined by conversion of [H-3] L-arginine to [H-3] L-citrulline, in STZ-induced diabetic rats was markedly lower than normal rats. Insulin treatment reversed the nNOS activity. Similar reversion by insulin treatment was also obtained in the gene expression of nNOS. However, the activity and gene expression of nNOS in glucose-challenged rats were not different from those in normal rats. The role of hyperglycemia can thus be ruled out. These findings indicated that an impairment of nNOS in the brain of rats with IDDM is mainly due to the absence of insulin. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 35]
机译：一氧化氮（NO）在胰岛素依赖性糖尿病（IDDM）的病理生理中起着重要作用。为了研究IDDM中胰岛素与NO的关系，本研究采用雄性Wistar大鼠通过静脉注射链脲佐菌素（STZ）诱导IDDM。使用四组大鼠。未治疗的正常对照组，胰岛素治疗的STZ组，媒介物治疗的STZ对照组和一组年龄匹配的大鼠（口服葡萄糖以增加血浆葡萄糖）补充了葡萄糖激发的大鼠。检查这些组小脑和肾脏中神经元一氧化氮合酶（nNOS）的活性和基因表达的变化。 STZ诱导的糖尿病大鼠中小脑nNOS的活性由[H-3] L-精氨酸转化为[H-3] L-瓜氨酸确定，其活性明显低于正常大鼠。胰岛素治疗可逆转nNOS活性。在nNOS的基因表达中也获得了类似的胰岛素治疗逆转。然而，葡萄糖激发的大鼠中nNOS的活性和基因表达与正常大鼠没有差异。因此可以排除高血糖的作用。这些发现表明，IDDM大鼠大脑中nNOS的损伤主要是由于缺乏胰岛素。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：35]

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