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两种胰岛素抵抗大鼠模型中脊髓激肽受体结合位点的增加。

Increases of spinal kinin receptor binding sites in two rat models of insulin resistance.

作者信息

El Midaoui Adil, Ongali Brice, Petcu Mihai, Rodi Donata, de Champlain Jacques, Neugebauer Witold, Couture Réjean

机构信息

Department of Physiology, Faculty of Medicine, Université de Montréal, C.P. 6128, Succ. Centre-ville, Montréal, Que., Canada H3C 3J7.

出版信息

Peptides. 2005 Aug;26(8):1323-30. doi: 10.1016/j.peptides.2005.03.028. Epub 2005 Apr 12.

DOI:10.1016/j.peptides.2005.03.028
PMID:16042974
Abstract

An autoradiographic study was conducted to determine whether kinin receptors are altered in the rat spinal cord in two experimental models of chronic hyperglycemia and insulin resistance. Sprague-Dawley rats were given 10% d-glucose in their drinking water alone or with insulin (9 mU/kg/min with osmotic pumps) for 4 weeks. Both groups and control rats were treated either with a normal chow diet or with an alpha-lipoic acid-supplemented diet as antioxidant therapy. After 4 weeks of treatment, glycemia, insulinemia, blood pressure, insulin resistance index, the production of superoxide anion in the aorta and the density of B2 receptor binding sites in the dorsal horn were significantly increased in the two models. These effects were prevented or attenuated by alpha-lipoic acid. In contrast, B2 receptor binding sites of most spinal cord laminae were increased in the glucose group only and were not affected by alpha-lipoic acid. Results show that chronic hyperglycemia associated with insulin resistance increases B1 and B2 receptor binding sites in the rat spinal cord through distinct mechanisms, including the oxidative stress for the B1 receptor.

摘要

进行了一项放射自显影研究,以确定在两种慢性高血糖和胰岛素抵抗的实验模型中,大鼠脊髓中的激肽受体是否发生改变。将斯普拉格-道利大鼠单独给予饮用水中的10% d-葡萄糖或与胰岛素(用渗透泵以9 mU/kg/分钟给药)一起给予4周。两组大鼠和对照大鼠均接受正常饲料饮食或补充α-硫辛酸的饮食作为抗氧化治疗。治疗4周后,两种模型中的血糖、胰岛素血症、血压、胰岛素抵抗指数、主动脉中超氧阴离子的产生以及背角中B2受体结合位点的密度均显著增加。这些作用被α-硫辛酸预防或减弱。相比之下,仅葡萄糖组中大多数脊髓板层的B2受体结合位点增加,且不受α-硫辛酸影响。结果表明,与胰岛素抵抗相关的慢性高血糖通过不同机制增加大鼠脊髓中的B1和B2受体结合位点,包括B1受体的氧化应激。

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引用本文的文献

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PLoS One. 2010 Sep 7;5(9):e12622. doi: 10.1371/journal.pone.0012622.
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Key role for spinal dorsal horn microglial kinin B1 receptor in early diabetic pain neuropathy.脊髓背角小胶质细胞激肽 B1 受体在早期糖尿病痛性神经病中的关键作用。
J Neuroinflammation. 2010 Jun 29;7(1):36. doi: 10.1186/1742-2094-7-36.
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Cellular localization of kinin B1 receptor in the spinal cord of streptozotocin-diabetic rats with a fluorescent [Nalpha-Bodipy]-des-Arg9-bradykinin.
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J Neuroinflammation. 2009 Mar 26;6:11. doi: 10.1186/1742-2094-6-11.
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The kinin B1 receptor antagonist SSR240612 reverses tactile and cold allodynia in an experimental rat model of insulin resistance.激肽B1受体拮抗剂SSR240612可逆转胰岛素抵抗实验大鼠模型中的触觉和冷觉异常性疼痛。
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