Literature DB >> 30850243

Effect of miR-132 on bupivacaine-induced neurotoxicity in human neuroblastoma cell line.

Huiying Zhang1, Jianzhong Lin2, Tingting Hu3, Zhiyun Ren4, Weiwan Wang4, Qiyue He5.   

Abstract

BACKGROUND: Local anesthetics (LAs) may generate neurotoxicity in neurons. In the current study, we explored the mechanisms by which microRNA-132 (miR-132) regulated the neurotoxicity of human neuroblastoma cells (SH-SY5Y) induced by bupivacaine (BUP).
METHODS: CCK-8, flow cytometry, EdU detection, qRT-PCR and western blotting were used to explore the cell viability, apoptosis and gene expression, respectively.
RESULTS: In this study, we found that 600 μM BUP dramatically inhibited SH-SY5Y cells viability. In addition, BUP induced cell apoptosis and neurotoxicity via increasing active caspase-3 and cleaved PARP1 levels. More importantly, the level of miR-132 was significantly up-regulated in BUP-treated cells, which was significantly reversed by miR-132 inhibitor. In addition, dual-luciferase assay indicated IGF1R was the directly binding target of miR-132 in cells. Our study further indicated that the level of IGF1R was markedly decreased by BUP interference, while miR-132 inhibitor exerted the opposite effect. Furthermore, BUP induced apoptosis and neurotoxicity in SH-SY5Y cells were attenuated by IGF1, which further confirmed IGF1R was the downstream target of BUP in SH-SY5Y cells.
CONCLUSION: In the present study, miR-132 played important roles in regulating BUP-induced neurotoxicity through IGF1R and may act as a promising molecular target for the treatment of human neurotoxicity induced by BUP.
Copyright © 2019 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Apoptosis; Bupivacaine; Neurotoxicity; miRNA

Mesh:

Substances:

Year:  2019        PMID: 30850243     DOI: 10.1016/j.jphs.2019.01.014

Source DB:  PubMed          Journal:  J Pharmacol Sci        ISSN: 1347-8613            Impact factor:   3.337


  11 in total

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