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Сyclooxygenase-2 Inhibitor Parecoxib Reduces LPS-Induced Activation of BV2 Microglia Cells
1Department of Anesthesiology, the People's Hospital of Longhua Shenzhen, Affiliated Longhua People's Hospital, Southern Medicine University, Shenzhen, China. lixiang1106@sina.com.
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.
Insights
Parecoxib, a cyclooxygenase-2 inhibitor, effectively prevents lipopolysaccharide (LPS)-induced activation of BV2 microglial cells. This inhibition involves suppressing the NLRP3 inflammasome pathway, reducing inflammatory markers.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia play a crucial role in neuroinflammation.
- Lipopolysaccharide (LPS) is a potent activator of microglial cells, inducing inflammatory responses.
- The NLRP3 inflammasome is a key mediator of inflammation in microglia.
Purpose of the Study:
- To investigate the inhibitory effect of parecoxib, a cyclooxygenase-2 (COX-2) inhibitor, on LPS-induced activation of BV2 microglial cells.
- To determine if parecoxib modulates the NLRP3 inflammasome pathway in activated microglia.
Main Methods:
- BV2 microglial cells were treated with LPS (1 μg/ml) to induce activation.
- Cells were pretreated with an optimal dose of parecoxib (80 μmol/liter) before LPS exposure.
- Cell morphology, proliferation, and the expression of NLRP3, caspase-1, pro-caspase-1, and IL-1β were assessed.
Main Results:
- LPS induced significant morphological changes and reduced proliferation in BV2 cells.
- Parecoxib pretreatment prevented LPS-induced alterations in cell morphology and proliferation.
- LPS significantly increased NLRP3 inflammasome activation and the expression of NLRP3, caspase-1, pro-caspase-1, and IL-1β.
- Parecoxib pretreatment effectively inhibited these LPS-induced increases in inflammatory markers.
Conclusions:
- Parecoxib demonstrates significant inhibitory effects on LPS-induced BV2 microglial activation.
- Parecoxib likely exerts its protective effects by inhibiting the activation of the NLRP3 inflammasome pathway.
- These findings suggest parecoxib as a potential therapeutic agent for neuroinflammatory conditions involving microglial activation.
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