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Dehydrocostus Lactone Down - regulates Lipopolysaccharide-induced SAA3 gene activation in the Microglia.

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Running Title: DDL inhibits the LPS-induced SAA3 gene expression in microgliaObjective: Research on the mechanism of Dehydrocostus lactone (DDL) in microglial cells of the brain needs to be improved, despite its reported anti-inflammatory, anticancer, and anti-proliferation properties as a natural product of Eerdun Wurile The precise functions of the Serum amyloid A (SAA) genes are not yet defined. However, these genes are suggested to possess antibacterial properties and can attract monocytes and neutrophils. On the other hand, SAA genes can also induce inflammatory cytokines and metalloproteinases in smooth muscle cells and macrophages, thus promoting inflammation. This study aimed to investigate the impact of DDL on SAA3 gene expression in microglial cells stimulated by LPS.Methods: The anti-inflammatory effects of DDL were studied using LPS-stimulated murine BV2 microglia. BV2 was cultured in DMEM, and then 4µM DDL was added. Then BV2 was treated with one ng/ml LPS for 24 hours to stimulate. Results: LPS treatment increased the expression of SAA3 mRNA in BV2 microglial cells, while DDL pre-treatment inhibited LPS-induced SAA3 mRNA expression.Conclusion: Microglia cells treated with LPS display a significant reduction in the expression of SAA3 gene transcripts upon treatment with DDL.
Title: Dehydrocostus Lactone Down - regulates Lipopolysaccharide-induced SAA3 gene activation in the Microglia.
Description:
Running Title: DDL inhibits the LPS-induced SAA3 gene expression in microgliaObjective: Research on the mechanism of Dehydrocostus lactone (DDL) in microglial cells of the brain needs to be improved, despite its reported anti-inflammatory, anticancer, and anti-proliferation properties as a natural product of Eerdun Wurile The precise functions of the Serum amyloid A (SAA) genes are not yet defined.
However, these genes are suggested to possess antibacterial properties and can attract monocytes and neutrophils.
On the other hand, SAA genes can also induce inflammatory cytokines and metalloproteinases in smooth muscle cells and macrophages, thus promoting inflammation.
This study aimed to investigate the impact of DDL on SAA3 gene expression in microglial cells stimulated by LPS.
Methods: The anti-inflammatory effects of DDL were studied using LPS-stimulated murine BV2 microglia.
BV2 was cultured in DMEM, and then 4µM DDL was added.
Then BV2 was treated with one ng/ml LPS for 24 hours to stimulate.
Results: LPS treatment increased the expression of SAA3 mRNA in BV2 microglial cells, while DDL pre-treatment inhibited LPS-induced SAA3 mRNA expression.
Conclusion: Microglia cells treated with LPS display a significant reduction in the expression of SAA3 gene transcripts upon treatment with DDL.

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