IMR Press / JIN / Volume 18 / Issue 4 / DOI: 10.31083/j.jin.2019.04.1138
Open Access Original Research
Effect of incubation with lipopolysaccharide and interferon-γ on reactive astrogliosis
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1 Department of Intensive Care Unit, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, P. R. China
*Correspondence: (Xiangyou Yu)
These authors contributed equally.
J. Integr. Neurosci. 2019, 18(4), 415–421;
Submitted: 30 July 2019 | Accepted: 18 October 2019 | Published: 30 December 2019
Copyright: © 2019 Hua et al. Published by IMR Press.
This is an open access article under the CC BY 4.0 license

Sepsis associated encephalopathy is a common complication of sepsis, but its pathogenesis of sepsis-associated encephalopathy remains unclear. Astrocytes are the most abundant brain glial cells, and reactive astrogliosis, a pathological response to central nervous system diseases, has a clear disease and disease-stage specificity. Functional changes of astrocytes are of great significance for the detection and prognosis of sepsis-associated encephalopathy. The pathogenesis of sepsis-associated encephalopathy was explored at the cellular level by examining astrogliosis in an in vitro model of sepsis-associated encephalopathy. Astrocytes of Wistar neonatal rats were incubated with different concentrations of lipopolysaccharide combined with interferon-γ. Cell viability was assessed by levels of tumor necrosis factor-α, interleukin-6, nitric oxide, reactive oxygen species, glial fibrillary acidic protein, changes of astrocyte morphology, and prevalence of apoptosis and necrosis. Compared with the control group, the cell viability of treated groups was decreased. The levels of tumor necrosis factor-α, interleukin-6, nitric oxide, reactive oxygen species, and glial fibrillary acidic protein were increased, hypertrophy of astrocytes was observed, and apoptosis was increased. The pathogenic outcomes of astrogliosis in sepsis-associated encephalopathy is discussed and a new tool provided to explore the pathogenesis of sepsis-associated encephalopathy at the cellular level.

sepsis-associated encephalopathy
glial fibrillary acidic protein
rat model
Figure 1.
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