中国神经再生研究(英文版)

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

糖基化终产物积累有关疾病中神经元的死亡及再生

  

  • 收稿日期:2014-03-19 出版日期:2014-04-15 发布日期:2014-04-15

Neuronal cell death and regeneration in diseases associated with advanced glycation end-products accumulation

Guzel Bikbova, Toshiyuki Oshitari, Shuichi Yamamoto   

  1. Department of Ophthalmology and Visual Science, Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba, Japan
  • Received:2014-03-19 Online:2014-04-15 Published:2014-04-15
  • Contact: Toshiyuki Oshitari, M.D., Ph.D., Department of Ophthalmology and Visual Science, Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba, Japan, Tarii@aol.com or oshitari@faculty.chiba-u.jp .
  • Supported by:

    This study is supported by a Grant-in Aid from the Ministry of Education, Science, Sports and Culture of the Japanese Government.

摘要:

越来越多的证据表明,早期糖尿病视网膜病变发病机制与神经元异常及神经元死亡有关。我们之前有关人类视网膜的研究表明,线粒体和胱天蛋白酶依赖的细胞死亡途径与糖尿病患者的视网膜神经细胞元变性的发病机制相关。来自日本千叶大学研究生医学院的Toshiyuki Oshitari教授等人研究证实对糖尿病应激诱导的视网膜神经元损伤中具有存活作用。同时他们也发现,在高糖条件下,神经营养素4具有最佳的神经保护和再生作用。在受损的视网膜神经节细胞(RGC的)中,胱天蛋白酶1,3, 8和9抑制剂培养视网膜的最大成活率为60%。因此,在视网膜培养过程中,受损的视网膜神经节细胞中至少会有40%的神经元死亡,它们与胱天蛋白酶非依赖性的细胞死亡机制有关。然而,较少有人深入关注在糖尿病应激包括糖基化终产物暴露条件下,半胱天冬酶依赖性细胞的死亡途径。

Abstract:

Growing evidence indicates that neuronal abnormalities including neuronal cell death are associated with the pathogenesis of early diabetic retinopathy. Our previous study of human retinas indicate that mitochondrial and caspase-dependent cell death pathways are associated with retinal neuronal cell degeneration in patients with diabetes Prof. Toshiyuki Oshitari from Chiba University Graduate School of Medicine in Japan had studied and showed a survival effect on damaged retinal neurons induced by diabetic stress. They also found that NT-4 had the best neuroprotective and regenerative effect under high glucose conditions. Earlier study indicated that the maximum rescue ratio of caspase-1, -3, -8, and -9 inhibitors in cultured retinas was 60% in damaged retinal ganglion cells (RGCs). Thus, at least 40% of neuronal cell death in damaged RGCs in cultured retinas should be related to caspase-independent cell death mechanisms. However, no reports have focused on caspase-independent cell death pathways under diabetic stress including AGEs exposure.