The protective effects of insulin-like growth factor-1 on neurochemical phenotypes of dorsal root ganglion neurons with BDE-209-induced neurotoxicity in vitro

Author:

Bai Xue1,Chen Tianhua1,Gao Yang2,Li Hao3,Li Zhenzhong1,Liu Zhen1

Affiliation:

1. Department of Anatomy, Shandong University School of Medicine, Jinan, China

2. Department of Human Biology, University of Toronto, Toronto, Ontario, Canada

3. Department of Orthopaedics, Shandong University Qilu Hospital, Jinan, China

Abstract

Polybrominated diphenyl ethers (PBDEs) exist extensively in the environment as contaminants, in which 2,2′,3,3′,4,4′,5,5′,6,6′-decabrominated diphenyl ether (BDE-209) is the most abundant PBDE found in human samples. BDE-209 has been shown to cause neurotoxicity of primary sensory neurons with few effective therapeutic options available. Here, cultured dorsal root ganglion (DRG) neurons were used to determine the therapeutic effects of insulin-like growth factor-1 (IGF-1) on BDE-209-induced neurotoxicity. The results showed that IGF-1 promoted neurite outgrowth and cell viability of DRG neurons with BDE-209-induced neurotoxicity. IGF-1 inhibited oxidative stress and apoptotic cell death caused by BDE-209 exposure. IGF-1 could reverse the decrease in growth-associated protein-43 (GAP-43) and calcitonin gene-related peptide (CGRP), but not neurofilament-200 (NF-200), expression resulting from BDE-209 exposure. The effects of IGF-1 could be blocked by the extracellular signal-regulated protein kinase (ERK1/2) inhibitor PD98059 and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002, either alone or in combination. IGF-1 may play an important role in neuroprotective effects on DRG neurons with BDE-209-induced neurotoxicity through inhibiting oxidative stress and apoptosis and regulating GAP-43 and CGRP expression of DRG neurons. Both ERK1/2 and PI3K/Akt signaling pathways were involved in the effects of IGF-1. Thus, IGF-1 might be one of the therapeutic agents on BDE-209-induced neurotoxicity.

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Public Health, Environmental and Occupational Health,Toxicology

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