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MicroRNA-96 is responsible for sevoflurane-induced cognitive dysfunction in neonatal rats via inhibiting IGF1R.
Brain Res Bull. 2019 01; 144:140-148.BR

Abstract

Sevoflurane is an experimental potent yet volatile anesthesia agent characterized by a low blood/gas partition coefficient. However, exposure to sevoflurane in neonatal mice has been speculated to result in learning deficits and abnormal social behavior. The aim of the present study was to investigate the relationship between sevoflurane and miR-96, in an attempt to identify the means by which it mediates IGF1R to influence the cognitive dysfunction (CD) in neonatal rats. Relationship between differentially expressed miRNAs and sevoflurane concentration was identified. The potential underlying regulatory mechanisms involved with sevoflurane were investigated through the administration of varying concentrations of the agent (1%, 2% and 4%), combined with miR-96 mimic or an inhibitor. A target prediction program was utilized, while the luciferase activity was determined in order to verify whether miR-96 targets IGF1R. The mRNA and protein levels of IGF1R, Bcl-2, Bax, and caspase-3 were measured followed by the determination of hippocampal neuron apoptosis. Learning and memory performance was assessed using the Morris water maze (MWM) test and step-down test. The obtained results highlighted a positive correlation between miR-96 and the concentration of sevoflurane, while miR-96 was confirmed to negatively target IGF1R. Our analyses indicated that 4% sevoflurane had a significantly stronger effect on reducing the levels of IGF1R and Bcl-2, while elevating the levels of miR-96, Bax and caspase-3 more so than that of 1% or 2% sevoflurane, which resulted in increased hippocampal neuron apoptosis but diminished the learning and memory performance of the rats. The addition of miR-96 mimic was demonstrated to exacerbate the influence of sevoflurane on hippocampal neurons as well as the cognitive function of the rats. The key findings of our study highlighted the role of miR-96 in the potential mechanism of sevoflurane anesthesia-induced CD in neonatal rats through the downregulation of IGF1R.

Authors+Show Affiliations

Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China. Electronic address: Weiy_sheng@126.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30217735

Citation

Xu, Chang, et al. "MicroRNA-96 Is Responsible for Sevoflurane-induced Cognitive Dysfunction in Neonatal Rats Via Inhibiting IGF1R." Brain Research Bulletin, vol. 144, 2019, pp. 140-148.
Xu C, Niu JJ, Zhou JF, et al. MicroRNA-96 is responsible for sevoflurane-induced cognitive dysfunction in neonatal rats via inhibiting IGF1R. Brain Res Bull. 2019;144:140-148.
Xu, C., Niu, J. J., Zhou, J. F., & Wei, Y. S. (2019). MicroRNA-96 is responsible for sevoflurane-induced cognitive dysfunction in neonatal rats via inhibiting IGF1R. Brain Research Bulletin, 144, 140-148. https://doi.org/10.1016/j.brainresbull.2018.09.001
Xu C, et al. MicroRNA-96 Is Responsible for Sevoflurane-induced Cognitive Dysfunction in Neonatal Rats Via Inhibiting IGF1R. Brain Res Bull. 2019;144:140-148. PubMed PMID: 30217735.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MicroRNA-96 is responsible for sevoflurane-induced cognitive dysfunction in neonatal rats via inhibiting IGF1R. AU - Xu,Chang, AU - Niu,Jiao-Jiao, AU - Zhou,Jun-Fei, AU - Wei,Yin-Sheng, Y1 - 2018/09/11/ PY - 2018/04/28/received PY - 2018/08/24/revised PY - 2018/09/07/accepted PY - 2018/9/16/pubmed PY - 2020/1/17/medline PY - 2018/9/16/entrez KW - Apoptosis KW - Cognitive dysfunction KW - Hippocampal neuron KW - IGF1R KW - MicroRNA-96 KW - Sevoflurane SP - 140 EP - 148 JF - Brain research bulletin JO - Brain Res. Bull. VL - 144 N2 - Sevoflurane is an experimental potent yet volatile anesthesia agent characterized by a low blood/gas partition coefficient. However, exposure to sevoflurane in neonatal mice has been speculated to result in learning deficits and abnormal social behavior. The aim of the present study was to investigate the relationship between sevoflurane and miR-96, in an attempt to identify the means by which it mediates IGF1R to influence the cognitive dysfunction (CD) in neonatal rats. Relationship between differentially expressed miRNAs and sevoflurane concentration was identified. The potential underlying regulatory mechanisms involved with sevoflurane were investigated through the administration of varying concentrations of the agent (1%, 2% and 4%), combined with miR-96 mimic or an inhibitor. A target prediction program was utilized, while the luciferase activity was determined in order to verify whether miR-96 targets IGF1R. The mRNA and protein levels of IGF1R, Bcl-2, Bax, and caspase-3 were measured followed by the determination of hippocampal neuron apoptosis. Learning and memory performance was assessed using the Morris water maze (MWM) test and step-down test. The obtained results highlighted a positive correlation between miR-96 and the concentration of sevoflurane, while miR-96 was confirmed to negatively target IGF1R. Our analyses indicated that 4% sevoflurane had a significantly stronger effect on reducing the levels of IGF1R and Bcl-2, while elevating the levels of miR-96, Bax and caspase-3 more so than that of 1% or 2% sevoflurane, which resulted in increased hippocampal neuron apoptosis but diminished the learning and memory performance of the rats. The addition of miR-96 mimic was demonstrated to exacerbate the influence of sevoflurane on hippocampal neurons as well as the cognitive function of the rats. The key findings of our study highlighted the role of miR-96 in the potential mechanism of sevoflurane anesthesia-induced CD in neonatal rats through the downregulation of IGF1R. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/30217735/MicroRNA_96_is_responsible_for_sevoflurane_induced_cognitive_dysfunction_in_neonatal_rats_via_inhibiting_IGF1R_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(18)30318-6 DB - PRIME DP - Unbound Medicine ER -