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

Park,Yang-Gyu; Jeong,Jae-Kyo; Lee,Ju-Hee; Lee,You-Jin; Seol,Jae-Won; Kim,Shang-Jin; Hur,Tai-Young; Jung,Young-Hun; Kang,Seog-Jin; Park,Sang-Youel

doi:10.3892/ijmm.2012.1198

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

Authors:
- Yang-Gyu Park
- Jae-Kyo Jeong
- Ju-Hee Lee
- You-Jin Lee
- Jae-Won Seol
- Shang-Jin Kim
- Tai-Young Hur
- Young-Hun Jung
- Seog-Jin Kang
- Sang-Youel Park
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Affiliations: Korea Zoonoses Research Institute, Bio-Safety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561-756, Republic of Korea, National Institute of Animal Science, Rural Development Administration, Cheonan, Chungnam 330-801, Republic of Korea
Published online on: November 29, 2012 https://doi.org/10.3892/ijmm.2012.1198
Pages: 325-330

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Abstract

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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