Insulin-like growth factor-1 protects against prion peptide-induced cell death in neuronal cells via inhibition of Bax translocation

被引：19

作者：

Park, Yang-Gyu ^{[1
]}

Jeong, Jae-Kyo ^{[1
]}

Moon, Myung-Hee ^{[1
]}

Lee, Ju-Hee ^{[1
]}

Lee, You-Jin ^{[1
]}

Seol, Jae-Won ^{[1
]}

Kim, Shang-Jin ^{[1
]}

Kang, Seog-Jin ^{[2
]}

Park, Sang-Youel ^{[1
]}

机构：

[1] Chonbuk Natl Univ, Korea Zoonoses Res Inst, Biosafety Res Inst, Coll Vet Med, Jeonju 561756, Jeonbuk, South Korea

[2] Rural Dev Adm, Technol Serv Div, Natl Inst Anim Sci, Suwon 441706, Gyeonggi Do, South Korea

来源：

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | 2012年 / 30卷 / 05期

关键词：

insul n-like growth factor-1; prion protein (106-126); prion disease; Bax; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; NEUROBLASTOMA-CELLS; PARKINSONS-DISEASE; SIGNALING PATHWAYS; INDUCED APOPTOSIS; INDUCTION; ACTIVATION; MEDIATORS; BRAINS;

D O I：

10.3892/ijmm.2012.1087

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Insulin-like growth factor-1 (IGF-1) is one of the most important components of bovine colostrum. It exhibits antiapoptotic and antioxidative activities. Prion diseases are neurodegenerative disorders caused by cell death through mitochondrial dysfunction and increasing generation of reactive oxygen species (ROS). This study examined the protective elect of IGF-1 on residues 106-126 of the cellular prion pretein [PrP (106-126)]-mediated mitochondrial neurotoxicity ad oxidative stress. In SH-SY5Y human neuronal cells, treatment with PrP (106-126) decreased the cell viability and IGF-1 pretreatment markedly blocked the PrP (106-126)-induced neuronal cell death. IGF-1 inhibited PrP (106-126)-induced intracellular ROS generation and mitochondrial oxidative stress. In addition, IGF-1 blocked the translocation of the Bax protein to the mitochondria induced by PrP (106-126). These results demonstrate that IGF-1 protects neuronal cells against PrP (106-126)-mediated neurotoxicity through an antioxidative effect and blockage of mitochondria1 Box translocation. The results also suggest that regulation of IGF-1 secretion may have a therapeutic potential in the management of mitochondrial dysfunction and oxidative stress-induced neurodegeneration.

引用

页码：1069 / 1074

页数：6

共 33 条

[1] Activation of the JNK-c-Jun pathway during the early phase of neuronal apoptosis induced by PrP106-126 and prion infection [J].