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Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate‑to‑severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs

  • Authors:
    • Xiping Yang
    • Yisheng Chen
    • Jianxin Li
    • Lijun Chen
    • Hefei Ren
    • Yang Liu
    • Xinyu Zhang

  • View Affiliations

  • Published online on: December 12, 2018     https://doi.org/10.3892/mmr.2018.9748
  • Pages: 1083-1091

  • Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Traumatic brain injury (TBI) is the most common cause of death and permanent disability in people aged <45, and is associated with secondary brain injury and bleed progression, resulting in increased morbidity and mortality. TBI may also induce innate host defense responses characterized by activation of resident microglia and astrocytes, brain microvascular endothelial cells and peripheral blood monocytes. In the present study, 34 patients with moderate‑to‑severe traumatic brain injury were randomly divided into two groups, including a 7.5% hypertonic saline (HS) treatment group (4 ml/kg) and 3% HS treatment group (4 ml/kg). The results demonstrated that treatment with 7.5% HS decreased the intracranial pressure and improved coagulofibrinolytic homeostasis. Analysis of the monocyte subsets revealed significant reduction in the proportion of cluster of differentiation (CD)14++CD16+ circulating inflammatory monocytes in the 7.5% HS group. In addition, 7.5% HS treatment downregulated the expression of long non‑coding (lnc) RNA2448‑11 and lncRNA1403 in the peripheral blood mononuclear cells of patients with TBI. Using reverse transcription‑quantitative polymerase chain reaction, it was determined that 7.5% HS regulated the expression of tumor necrosis factor‑α, interleukin‑1β, transforming growth factor‑β and thrombomodulin, which are the target genes of lncRNA2448‑11 and lncRNA1403. These results indicated that 7.5% HS improved the intracranial pressure and coagulofibrinolytic homeostasis by modulating the phenotype of monocytes through lncRNA2448‑11 and lncRNA1403. These findings provided evidence that initial resuscitation with HS imparts functional changes to inflammatory cells following TBI, thereby reducing potential neuroinflammatory events associated with secondary brain injury.
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February-2019
Volume 19 Issue 2

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

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  • Ranked Medicine Research and Experimental
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  • CiteScore: 7.6
  • CiteScore Rank: Q1: #82/347 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.647
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Spandidos Publications style
Yang X, Chen Y, Li J, Chen L, Ren H, Liu Y and Zhang X: Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate‑to‑severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs. Mol Med Rep 19: 1083-1091, 2019.
APA
Yang, X., Chen, Y., Li, J., Chen, L., Ren, H., Liu, Y., & Zhang, X. (2019). Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate‑to‑severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs. Molecular Medicine Reports, 19, 1083-1091. https://doi.org/10.3892/mmr.2018.9748
MLA
Yang, X., Chen, Y., Li, J., Chen, L., Ren, H., Liu, Y., Zhang, X."Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate‑to‑severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs". Molecular Medicine Reports 19.2 (2019): 1083-1091.
Chicago
Yang, X., Chen, Y., Li, J., Chen, L., Ren, H., Liu, Y., Zhang, X."Hypertonic saline maintains coagulofibrinolytic homeostasis following moderate‑to‑severe traumatic brain injury by regulating monocyte phenotype via expression of lncRNAs". Molecular Medicine Reports 19, no. 2 (2019): 1083-1091. https://doi.org/10.3892/mmr.2018.9748