首页    期刊浏览 2024年12月01日 星期日
登录注册

文章基本信息

  • 标题: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
  • 本地全文:下载
  • 作者:Yukinori Shimoshige ; Ryugo Enomoto ; Toshiaki Aoki
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:2010
  • 卷号:33
  • 期号:1
  • 页码:67-71
  • DOI:10.1248/bpb.33.67
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要: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 Tα1 α-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 βIII 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.
  • 关键词:aldose reductase inhibitor;diabetic neuropathy;dorsal root ganglia;neurotrophin;neuronal cytoskeletal protein
国家哲学社会科学文献中心版权所有