ArticleBulletin of experimental biology and medicine2022
Сyclooxygenase-2 Inhibitor Parecoxib Reduces LPS-Induced Activation of BV2 Microglia Cells.
Article in Bulletin of experimental biology and medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Downregulation of Gbp2 Attenuates LPS-Induced Inflammation in BV2 Microglia Cells Through Inhibition of STAT1.Journal of inflammation research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied the inhibitory effect of cyclooxygenase-2 inhibitor parecoxib on LPS-induced activation of BV2 microglia cells. The optimal dose of parecoxib (80 μmol/liter) was evaluated by the Cell Counting Kit-8. The cells were divided into the following groups: control (intact cells without treatment); LPS (treatment with 1 μg/ml LPS for 6 h), and experimental (pretreatment with 80 μmol/liter parecoxib for 24 h followed by incubation with 1 μg/ml LPS for 6 h). Cell morphology and proliferation and the expression of NLRP3, caspase-1, pro-caspase-1, and IL-1β were assessed. LPS induced significant morphological changes and decreased proliferation of primary BV2 cells in comparison with the control. These changes were prevented by parecoxib pretreatment. LPS significantly increased NLRP3 inflammatory vesicle activation and expression of NLRP3, caspase-1, pro-caspase-1, and IL-1β in comparison with the control group; pretreatment with parecoxib prevented all these changes. Our results suggest that pretreatment with parecoxib inhibited LPS-induced activation of BV2 microglial cells and probably inhibited NLRP3 inflammasome activation.
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Registered trials
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