Open Access

Isoflurane exposure regulates the cell viability and BDNF expression of astrocytes via upregulation of TREK‑1

  • Authors:
    • Cui‑Hong Zhou
    • Ya‑Hong Zhang
    • Fen Xue
    • Shan‑Shan Xue
    • Yun‑Chun Chen
    • Ting Gu
    • Zheng‑Wu Peng
    • Hua‑Ning Wang
  • View Affiliations

  • Published online on: September 20, 2017     https://doi.org/10.3892/mmr.2017.7547
  • Pages: 7305-7314
  • Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Neonatal isoflurane exposure in rodents disrupts hippocampal cognitive functions, including learning and memory, and astrocytes may have an important role in this process. However, the molecular mechanisms underlying this disruption are not fully understood. The present study investigated the role of TWIK‑related K+ channel (TREK‑1) in isoflurane‑induced cognitive impairment. Lentiviruses were used to overexpress or knockdown TREK‑1 in astrocytes exposed to increasing concentrations of isoflurane or O2 for 2 h. Subsequently, the mRNA and protein expression of brain‑derived neurotrophic factor (BDNF), caspase‑3, Bcl‑2‑associated X (Bax) and TREK‑1 was measured by reverse transcription‑ quantitative polymerase chain reaction and western blot analysis, respectively. In addition, cell viability was assessed by a 2‑(4‑Iodophenyl)‑3‑(4‑nitrophenyl)‑5‑(2,4‑disulfophenyl)‑ 2H‑tetrazolium monosodium salt assay. The results demonstrated that, prior to manipulating TREK‑1, isoflurane significantly decreased the cell viability and BDNF expression, and increased Bax, caspase‑3 and TREK‑1 expression was observed. However, TREK‑1 overexpression in astrocytes significantly downregulated BDNF expression, and upregulated Bax and caspase‑3 expression. Furthermore, lentiviral‑mediated short hairpin RNA knockdown of TREK‑1 effectively inhibited the isoflurane‑induced changes in BDNF, Bax and caspase‑3 expression. Taken together, the results of the present study indicate that isoflurane‑induced cell damage in astrocytes may be associated with TREK‑1‑mediated inhibition of BDNF and provide a reference for the safe use of isoflurane anesthesia in infants and children.
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November-2017
Volume 16 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Zhou CH, Zhang YH, Xue F, Xue SS, Chen YC, Gu T, Peng ZW and Wang HN: Isoflurane exposure regulates the cell viability and BDNF expression of astrocytes via upregulation of TREK‑1. Mol Med Rep 16: 7305-7314, 2017.
APA
Zhou, C., Zhang, Y., Xue, F., Xue, S., Chen, Y., Gu, T. ... Wang, H. (2017). Isoflurane exposure regulates the cell viability and BDNF expression of astrocytes via upregulation of TREK‑1. Molecular Medicine Reports, 16, 7305-7314. https://doi.org/10.3892/mmr.2017.7547
MLA
Zhou, C., Zhang, Y., Xue, F., Xue, S., Chen, Y., Gu, T., Peng, Z., Wang, H."Isoflurane exposure regulates the cell viability and BDNF expression of astrocytes via upregulation of TREK‑1". Molecular Medicine Reports 16.5 (2017): 7305-7314.
Chicago
Zhou, C., Zhang, Y., Xue, F., Xue, S., Chen, Y., Gu, T., Peng, Z., Wang, H."Isoflurane exposure regulates the cell viability and BDNF expression of astrocytes via upregulation of TREK‑1". Molecular Medicine Reports 16, no. 5 (2017): 7305-7314. https://doi.org/10.3892/mmr.2017.7547