Lactoferrin protects against prion protein-induced cell death in neuronal cells by preventing mitochondrial dysfunction

Int J Mol Med. 2013 Feb;31(2):325-30. doi: 10.3892/ijmm.2012.1198. Epub 2012 Nov 29.


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).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cattle
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Humans
  • Lactoferrin / therapeutic use*
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Mitochondria / pathology
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neurons / pathology
  • Oxidative Stress / drug effects
  • Peptide Fragments / toxicity*
  • Prion Diseases / metabolism
  • Prion Diseases / pathology
  • Prion Diseases / prevention & control*
  • Prions / toxicity*
  • Reactive Oxygen Species / metabolism*


  • Peptide Fragments
  • Prions
  • Reactive Oxygen Species
  • prion protein (106-126)
  • Lactoferrin