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The protective effects of insulin-like growth factor-1 on neurochemical phenotypes of dorsal root ganglion neurons with BDE-209-induced neurotoxicity in vitro.
Toxicol Ind Health. 2017 Mar; 33(3):250-264.TI

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.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27090441

Citation

Bai, Xue, et al. "The Protective Effects of Insulin-like Growth Factor-1 On Neurochemical Phenotypes of Dorsal Root Ganglion Neurons With BDE-209-induced Neurotoxicity in Vitro." Toxicology and Industrial Health, vol. 33, no. 3, 2017, pp. 250-264.
Bai X, Chen T, Gao Y, et al. The protective effects of insulin-like growth factor-1 on neurochemical phenotypes of dorsal root ganglion neurons with BDE-209-induced neurotoxicity in vitro. Toxicol Ind Health. 2017;33(3):250-264.
Bai, X., Chen, T., Gao, Y., Li, H., Li, Z., & Liu, Z. (2017). The protective effects of insulin-like growth factor-1 on neurochemical phenotypes of dorsal root ganglion neurons with BDE-209-induced neurotoxicity in vitro. Toxicology and Industrial Health, 33(3), 250-264. https://doi.org/10.1177/0748233716638004
Bai X, et al. The Protective Effects of Insulin-like Growth Factor-1 On Neurochemical Phenotypes of Dorsal Root Ganglion Neurons With BDE-209-induced Neurotoxicity in Vitro. Toxicol Ind Health. 2017;33(3):250-264. PubMed PMID: 27090441.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The protective effects of insulin-like growth factor-1 on neurochemical phenotypes of dorsal root ganglion neurons with BDE-209-induced neurotoxicity in vitro. AU - Bai,Xue, AU - Chen,Tianhua, AU - Gao,Yang, AU - Li,Hao, AU - Li,Zhenzhong, AU - Liu,Zhen, Y1 - 2016/07/10/ PY - 2016/4/20/pubmed PY - 2017/6/7/medline PY - 2016/4/20/entrez KW - Insulin-like growth factor-1 KW - dorsal root ganglion KW - neuron KW - neurotoxicity KW - polybrominated diphenyl ether SP - 250 EP - 264 JF - Toxicology and industrial health JO - Toxicol Ind Health VL - 33 IS - 3 N2 - 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. SN - 1477-0393 UR - https://www.unboundmedicine.com/medline/citation/27090441/The_protective_effects_of_insulin_like_growth_factor_1_on_neurochemical_phenotypes_of_dorsal_root_ganglion_neurons_with_BDE_209_induced_neurotoxicity_in_vitro_ L2 - http://journals.sagepub.com/doi/full/10.1177/0748233716638004?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -