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Author Notes:

Correspondence: luozq1962@163.com; shaojieyue@163.com

CC participated in ELISA, flow cytometry, western blotting and real-time RT-PCR detection and drafted the manuscript.

ZCL, NZ, HH and MW participated in the isolation and treatment of astrocytes and detection of brain water content.

GJ and HS participated in the design of the study and performed the statistical analysis.

SY, ZL and XY conceived of the study, and participated in its design and coordination and helped to draft the manuscript.

All authors read and approved the final manuscript.

The authors declare that they have no competing interests.

Subjects:

Research Funding:

This study was supported by grants from the National Natural Science Foundation of China (No: 81070970), Specialized Research Fund for the Doctoral Program of Higher Education (No: 20090162110016), the Open-End Fund for the Valuable and Precision Instruments of Central South University and Research Fund of Development and Research Fund of Development and Reform Commission of Hunan Province (No:2010).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Critical Care Medicine
  • General & Internal Medicine
  • CRITICAL CARE MEDICINE
  • hypertonic saline
  • lipopolysaccharide
  • brain edema
  • aquaporin 4
  • protein kinase C
  • interleukin 1 beta
  • PROTEIN-KINASE-C
  • INCREASED INTRACRANIAL-PRESSURE
  • EXPERIMENTAL INTRACEREBRAL HEMORRHAGE
  • PHORBOL-MYRISTATE ACETATE
  • CEREBRAL EDEMA
  • 20-PERCENT MANNITOL
  • RAT-BRAIN
  • SEPTIC ENCEPHALOPATHY
  • BARRIER DISRUPTION
  • PLASMA-MEMBRANES

Hypertonic saline reduces lipopolysaccharide-induced mouse brain edema through inhibiting aquaporin 4 expression

Tools:

Journal Title:

Critical Care Nursing Quarterly

Volume:

Volume 16, Number 5

Publisher:

, Pages R186-R186

Type of Work:

Article | Final Publisher PDF

Abstract:

Introduction: Three percent sodium chloride (NaCl) treatment has been shown to reduce brain edema and inhibited brain aquaporin 4 (AQP4) expression in bacterial meningitis induced by Escherichia coli. Lipopolysaccharide (LPS) is the main pathogenic component of E. coli. We aimed to explore the effect of 3% NaCl in mouse brain edema induced by LPS, as well as to elucidate the potential mechanisms of action. Methods: Three percent NaCl was used to treat cerebral edema induced by LPS in mice in vivo. Brain water content, IL-1β, TNFα, immunoglobulin G (IgG), AQP4 mRNA and protein were measured in brain tissues. IL-1β, 3% NaCl and calphostin C (a specific inhibitor of protein kinase C) were used to treat the primary astrocytes in vitro. AQP4 mRNA and protein were measured in astrocytes. Differences in various groups were determined by one-way analysis of variance. Results: Three percent NaCl attenuated the increase of brain water content, IL-1β, TNFα, IgG, AQP4 mRNA and protein in brain tissues induced by LPS. Three percent NaCl inhibited the increase of AQP4 mRNA and protein in astrocytes induced by IL-1β in vitro. Calphostin C blocked the decrease of AQP4 mRNA and protein in astrocytes induced by 3% NaCl in vitro. Conclusions: Osmotherapy with 3% NaCl ameliorated LPS-induced cerebral edema in vivo. In addition to its osmotic force, 3% NaCl exerted anti-edema effects possibly through down-regulating the expression of proinflammatory cytokines (IL-1β and TNFα) and inhibiting the expression of AQP4 induced by proinflammatory cytokines. Three percent NaCl attenuated the expression of AQP4 through activation of protein kinase C in astrocytes.

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© 2012 Cao et al.; licensee BioMed Central Ltd.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 2.0 Generic License (http://creativecommons.org/licenses/by/2.0/).

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