Mitochondrial Ferritin Deletion Exacerbates β-Amyloid-Induced Neurotoxicity in Mice

作者：Wang, Peina; Wu, Qiong; Wu, Wenyue; Li, Haiyan; Guo, Yuetong; Yu, Peng; Gao, Guofen; Shi, Zhenhua; Zhao, Baolu; Chang, Yan-Zhong^*

来源：Oxidative Medicine and Cellular Longevity, 2017, 2017: 1020357.

DOI：10.1155/2017/1020357

• ALZHEIMERS-DISEASE
• MEMORY DEFICITS
• OXIDATIVE STRESS
• ANIMAL-MODEL
• CELL-DAMAGE
• IRON
• PROTEIN
• POLYPHENOLS
• IMPAIRMENT
• METABOLISM

Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates beta-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on beta-myloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with A beta(25-35) to establish an Alzheimer's disease model. Knockout of Ftmt significantly exacerbated A beta(25-35)-induced learning and memory impairment. The Bcl-2/Bax ratio inmouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. IncreasedMDA levels were also detected in Ftmt knockout mice treated with A beta(25-35). In conclusion, this study demonstrated that the neurological impairment induced by A beta(25-35) was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress.

• 出版日期2017
• 单位河北师范大学