Corticosterone potentiates ochratoxin A-induced microglial activation
Issued Date
2022-01-01
Resource Type
ISSN
18685021
eISSN
1868503X
Scopus ID
2-s2.0-85128515950
Pubmed ID
35437979
Journal Title
Biomolecular Concepts
Volume
13
Issue
1
Start Page
230
End Page
241
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomolecular Concepts Vol.13 No.1 (2022) , 230-241
Suggested Citation
Chansawhang A. Corticosterone potentiates ochratoxin A-induced microglial activation. Biomolecular Concepts Vol.13 No.1 (2022) , 230-241. 241. doi:10.1515/bmc-2022-0017 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/86747
Title
Corticosterone potentiates ochratoxin A-induced microglial activation
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Microglial activation in the central nervous system (CNS) has been associated with brain damage and neurodegenerative disorders. Ochratoxin A (OTA) is a mycotoxin that occurs naturally in food and feed and has been associated with neurotoxicity, while corticosteroids are CNS' physiological function modulators. This study examined how OTA affected microglia activation and how corticosteroids influenced microglial neuroinflammation. Murine microglial cells (BV-2) were stimulated by OTA, and the potentiation effects on OTA-induced inflammation were determined by corticosterone pre-treatment. Expressions of pro-inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) were determined. Phosphorylation of mitogen-activated protein kinases (MAPKs) was analyzed by western blotting. OTA significantly increased the mRNA expression of IL-6, TNF-α, IL-1β, and iNOS and also elevated IL-6 and NO levels. Corticosterone pre-treatment enhanced the neuroinflammatory response to OTA in a mineralocorticoid receptor (MR)-dependent mechanism, which is associated with increases in extracellular signal-regulated kinase (ERK) and p38 MAPK activation. In response to OTA, microglial cells produced pro-inflammatory cytokines and NO, while corticosterone increased OTA-induced ERK and p38 MAPK phosphorylation via MR. Findings indicated the direct role of OTA in microglia activation and neuroinflammatory response and suggested that low corticosterone concentrations in the brain exacerbated neurodegeneration.