期刊
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 31, 期 2, 页码 325-330出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2012.1198
关键词
lactoferrin; PrP (106-126); prion disease; reactive oxygen species scavenger
资金
- Cooperative Research Program for Agriculture Science and Technology Development in Rural Development Administration [PJ907116]
- National Research Foundation of the Korea
- Korean Government [2010-E00019]
Prion disorder-related neurodegenerative diseases are characterized by the accumulation of prion protein (PrP) scrapie isoform (PrPsc) within the central nervous system. PrPsc induces neuronal cell death by increasing intracellular generation of reactive oxygen species (ROS). Lactoferrin (LF) is an 80 kDa protein, which has antioxidant abilities due to the scavenging of ROS. The effects of LF treatment on PrP (106-126)-mediated neurotoxicity and ROS generation were the focus of this study. LF treatment protected against PrP (106-126)-induced neuronal cell death and decreased ROS generation. The reduced ROS generation prevented PrP (106-126)-induced mitochondrial dysfunction. Moreover, PrP (106-126)-induced protein activation including c-Jun N-terminal kinase and caspase-3 were blocked by LF treatment. These results demonstrated that LF protects neuronal cells against PrP (106-126)-mediated neurotoxicity through the scavenging of ROS and provide evidence that LF treatment prevents neuronal cell death caused by PrP (106-126).
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