Neuroprotective effect and adult optic nerve regeneration of administration of tacrolimus against spontaneous neuropathy in NF-kBp50-dificient mice as a normal tension glaucoma model

转录因子核因子-kappa B（NF-kB）/Rel家族可能参与神经元细胞的死亡和存活。我们报道了NF -κ Bp 50缺陷小鼠表现出许多类似于人类正常眼压性青光眼（NTG）的特征.我们的目的是阐明NTG的启动机制。钙调磷酸酶抑制剂他克莫司长期给药可显著降低慢性视神经病变。我们还研究了长期给予他克莫司的p50缺陷小鼠中视网膜细胞是否具有产生神经元的潜力。他克莫司治疗显着促进双极细胞衍生的视网膜祖细胞的增殖和视神经再生损伤后或在视网膜神经节细胞变性的p50-deficientmice.These实验结果提出视神经愈合和碱性成纤维细胞生长因子（bFGF）的表达，通过长期给药他克莫司。

The transcription factor nuclear factor-kappa B (NF-kB)/Rel family may be involved in neuronal cell death and survival. We reported that NF -kBp50-deficient mice exhibit many features resembling human normal tension glaucoma (NTG). Our aim is to elucidate the mechanism of the initiation of NTG. Chronic optic neuropathy was significantly reduced under chronic administration of calcineurin inhibitor Tacrolimus. We have also investigated whether retinal cells have the potential to generate neurons in p50-deficient mice with chronic administration of Tacrolimus. Tacrolimus-treatment markedly promotes the proliferation of bipolar cell-derived retinal progenitors and optic nerve regeneration after damage to or during the degeneration of retinal ganglion cells in p50-deficient mice.These experimental results proposed optic nerve healing and basic fibroblast growth factor (bFGF) expression by the chronic administration of Tacrolimus.