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醛糖还原酶在链脲佐菌素诱导的糖尿病大鼠背根神经节神经营养因子受体和神经元细胞骨架蛋白 mRNA 水平改变中的作用。

The involvement of aldose reductase in alterations to neurotrophin receptors and neuronal cytoskeletal protein mRNA levels in the dorsal root ganglion of streptozotocin-induced diabetic rats.

机构信息

Pharmacology Research Labs, Astellas Pharma Inc., Tsukuba, Ibaraki 305-8585, Japan.

出版信息

Biol Pharm Bull. 2010;33(1):67-71. doi: 10.1248/bpb.33.67.

Abstract

Dorsal root ganglia (DRG) are recognized as one of the organs which are damaged in peripheral sensory diabetic neuropathy. In an experimental animal model, the alteration of the mRNA expression level of neurotrophins, their receptors and neuronal cytoskeletal protein have been reported. In this study, we examined whether these changes are improved by treatment with the aldose reductase inhibitor, zenarestat, in early-stage diabetic neuropathy of streptozotocin (STZ)-induced diabetic rats. Two weeks after the induction of diabetes mellitus by STZ treatment, zenarestat or a vehicle were given orally for two weeks. After the zenarestat treatment, the mRNA expression levels of neurotrophin receptors and neuronal cytoskeletal proteins in dorsal root ganglia were determined with a real-time polymerase chain reaction (PCR) method. Compared with the expression level of normal rats, a significant increase in Trk-C and Talpha1 alpha-tubulin and a decrease in neurofilament H mRNA expression level were observed in the DRG of STZ rats, while there were no significant changes in Trk-A, Trk-B, p75, neurofilament L, neurofilament M and betaIII tubulin mRNA expression. Zenarestat treatment significantly ameliorated the abnormal increase in Trk-C mRNA expression level. These data suggest that hyperactivation of the polyol pathway induces a deficit in neurotropism on peripheral sensory diabetic neuropathy.

摘要

背根神经节 (DRG) 被认为是外周感觉性糖尿病神经病变受损的器官之一。在实验动物模型中,已经报道了神经营养因子及其受体和神经元细胞骨架蛋白的 mRNA 表达水平的改变。在这项研究中,我们检查了醛糖还原酶抑制剂 zenarestat 是否可以改善链脲佐菌素 (STZ) 诱导的糖尿病大鼠早期糖尿病神经病变中的这些变化。用 STZ 处理诱导糖尿病 2 周后,给予 zenarestat 或载体口服 2 周。zenarestat 治疗后,用实时聚合酶链反应 (PCR) 法测定背根神经节中神经营养因子受体和神经元细胞骨架蛋白的 mRNA 表达水平。与正常大鼠的表达水平相比,在 STZ 大鼠的 DRG 中观察到 Trk-C 和 Talpha1 α-微管蛋白的 mRNA 表达水平显著增加,而神经丝 H 的 mRNA 表达水平降低,而 Trk-A、Trk-B、p75、神经丝 L、神经丝 M 和 βIII 微管蛋白的 mRNA 表达水平没有显著变化。zenarestat 治疗显著改善了 Trk-C mRNA 表达水平的异常增加。这些数据表明,多元醇途径的过度激活导致外周感觉性糖尿病神经病变中的神经营养缺陷。

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