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Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κB/Hif-1α Signaling.
- Source :
- BioMed Research International; 4/28/2020, p1-11, 11p
- Publication Year :
- 2020
-
Abstract
- Hypoxia-induced neuroinflammation typically causes neurological damage and can occur during stroke, neonatal hypoxic-ischemic encephalopathy, and other diseases. Propofol is widely used as an intravenous anesthetic. Studies have shown that propofol has antineuroinflammatory effect. However, the underlying mechanism remains to be fully elucidated. Thus, we aimed to investigate the beneficial effects of propofol against hypoxia-induced neuroinflammation and elucidated its potential cellular and biochemical mechanisms of action. In this study, we chose cobalt chloride (CoCl<subscript>2</subscript>) to establish a hypoxic model. We found that propofol decreased hypoxia-induced proinflammatory cytokines (TNFα, IL-1β, and IL-6) in BV2 microglia, significantly suppressed the excessive production of reactive oxygen species, and increased the total antioxidant capacity and superoxide dismutase activity. Furthermore, propofol attenuated the hypoxia-induced decrease in mitochondrial membrane potential andy 2 strongly inhibited protein expression of nuclear factor-kappa B (NF-κB) subunit p65 and hypoxia inducible factor-1α (Hif-1α) in hypoxic BV2 cells. To investigate the role of NF-κB p65, specific small interfering RNA (siRNA) against NF-κB p65 were transfected into BV2 cells, followed by exposure to hypoxia for 24 h. Hypoxia-induced Hif-1α production was downregulated after NF-κB p65 silencing. Further, propofol suppressed Hif-1α expression by inhibiting the upregulation of NF-κB p65 after exposure to hypoxia in BV2 microglia. In summary, propofol attenuates hypoxia-induced neuroinflammation, at least in part by inhibiting oxidative stress and NF-κB/Hif-1α signaling. [ABSTRACT FROM AUTHOR]
- Subjects :
- INFLAMMATION prevention
NEUROLOGICAL disorder prevention
REACTIVE oxygen species
HYPOXEMIA
CELL membranes
CELLULAR signal transduction
CHLORIDES
COBALT
GENE expression
INFLAMMATION
INTERLEUKINS
MITOCHONDRIA
NEUROLOGICAL disorders
NEUROGLIA
RNA
SUPEROXIDE dismutase
TRANSCRIPTION factors
TUMOR necrosis factors
DNA-binding proteins
OXIDATIVE stress
PROPOFOL
DISEASE complications
PHARMACODYNAMICS
Subjects
Details
- Language :
- English
- ISSN :
- 23146133
- Database :
- Complementary Index
- Journal :
- BioMed Research International
- Publication Type :
- Academic Journal
- Accession number :
- 142945888
- Full Text :
- https://doi.org/10.1155/2020/8978704