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Updated: May 5, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
[Immune regulatory effect of citalopram on microglial cells]
Shanshan Wang1, Haiying Chen, Hengge Xie
1Department of Neurology, Nanlou Clinical Division, PLA General Hospital, Beijing 100853, China.
Objective:
To investigate the effects of antidepressant citalopram on the gene expressions of tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL-1β), and to discuss the impacts of citalopram on p38 and c-jun N-terminal kinase (JNK) of mitogen-activated protein kinase (MAPK) family in microglial cells.
Methods:
BV2 cells were induced by lipopolysaccharide (LPS) to produce TNF-α and IL-1β. After pretreatment with citalopram (20 μmol/L) for 4 h, the mRNA levels of TNF-α and IL-1β were measured by quantitative real-time PCR (qRT-PCR); after pretreatment for 24 h, the protein levels of TNF-α and IL-1β were analyzed by ELISA; the effects of citalopram on the phosphorylation of p38MAPK and JNK were observed after pretreatment for 30 min.
Results:
Citalopram significantly inhibited the mRNA and protein expressions of TNF-α and IL-1β, and the phosphorylation of p38MAPK and JNK.
Conclusion:
Citalopram may play the anti-inflammatory role by inhibiting MAPK pathway in microglial cells.
