He Xi-Jun, Uchida Kazuyuki, Megumi Chiaki, Tsuge Nobuaki, Nakayama Hiroyuki
State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001 People's Republic of China ; Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi,Bunkyo-ku, Tokyo 113-8657, Japan.
Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi,Bunkyo-ku, Tokyo 113-8657, Japan.
J Toxicol Pathol. 2015 Oct;28(4):197-206. doi: 10.1293/tox.2015-0020. Epub 2015 Jul 27.
Studies in vivo and in vitro suggest that curcumin is a neuroprotective agent. Experiments were conducted to determine whether dietary supplementation with curcumin has neuroprotective effects in a mouse model of Parkinson's disease (PD). Treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) significantly induced the loss of dopaminergic cells in the substantia nigra and deletion of dopamine in the striatum, which was attenuated by long-term (7 weeks) dietary supplementation with curcumin at a concentration of 0.5% or 2.0% (w/w). Although curcumin did not prevent the MPTP-induced apoptosis of neuroblasts in the subventricular zone (SVZ), it promoted the regeneration of neuroblasts in the anterior part of the SVZ (SVZa) at 3 days after MPTP treatment. Furthermore, curcumin enhanced the MPTP-induced activation of microglia and astrocytes in the striatum and increased the expression of glial cell line-derived neurotrophic factor (GDNF) and transforming growth factor-β1 (TGFβ1) in the striatum and SVZ. GDNF and TGFβ1 are thought to play an important role in protecting neurons from injury in the central and peripheral nervous systems. These results suggest that long-term administration of curcumin blocks the neurotoxicity of MPTP in the nigrostriatal dopaminergic system of the mouse and that the neuroprotective effect might be correlated with the increased expression of GDNF and TGFβ1. Curcumin may be effective in preventing or slowing the progression of PD.
体内和体外研究表明,姜黄素是一种神经保护剂。开展实验以确定在帕金森病(PD)小鼠模型中,饮食补充姜黄素是否具有神经保护作用。用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理显著诱导黑质中多巴胺能细胞的损失以及纹状体中多巴胺的缺失,而长期(7周)饮食补充浓度为0.5%或2.0%(w/w)的姜黄素可使其减轻。虽然姜黄素不能阻止MPTP诱导的脑室下区(SVZ)神经母细胞凋亡,但在MPTP处理后3天,它促进了SVZ前部(SVZa)神经母细胞的再生。此外,姜黄素增强了MPTP诱导的纹状体中小胶质细胞和星形胶质细胞的激活,并增加了纹状体和SVZ中胶质细胞源性神经营养因子(GDNF)和转化生长因子-β1(TGFβ1)的表达。GDNF和TGFβ1被认为在保护中枢和外周神经系统中的神经元免受损伤方面发挥重要作用。这些结果表明,长期给予姜黄素可阻断MPTP对小鼠黑质纹状体多巴胺能系统的神经毒性,且这种神经保护作用可能与GDNF和TGFβ1表达增加有关。姜黄素可能对预防或减缓PD的进展有效。