| Cell Research: |
| China Journal of Traditional Chinese Medicine & Pharmacy, 2016(05). | | Astragaloside I inhibited the activation of BV-2 cell induced by LPS through modulation of PI3K/Akt/NF-κB pathway[Reference: WebLink] | To investigate the effect and mechanism of Astragaloside I(AST I) on the activation of microglial cell line BV-2 induced by LPS.
METHODS AND RESULTS:
After pre-treated with AST I(25, 50, 100μmol/L) for 2 h, BV-2 cells were stimulated with LPS(200ng/m L) for 20 h. Thereafter, the cells and the culture medium were collected. Cell viability was measured by CCK-8 method. Concentration of TNF-α was detected by using ELISA kit. Secretion of NO in medium was assayed with Greiss approach. Gene expressions of CD11 b, TNF-α, i NOS, and IL-1β m RNA were detected with quantitative PCR. Protein expression of PI3K/Akt/NF-κB pathway was detected using Western blotting assay. Neuclear translocation of p-NF-κB was monitored with immunocytochemistry. AST I inhibited the secretion of TNF-α and NO on BV-2 cells upon LPS stimulation(P0.001) without affecting cell viability. It could prevent the up-regulation of gene expressions of TNF-α, i NOS and IL-1β(P0.001, P0.001, P0.05) but not that of CD11 b. Meanwhile, AST I suppressed the increase of i NOS and COX-2 protein induced by LPS. Further study disclosed that AST I reduced nuclear translocation of activated NF-κB and deceased phosphorylation of PI3 K, Akt, NF-κB, and IκB.
CONCLUSIONS:
Astragaloside I inhibited the activation of BV-2 cells induced by LPS through suppressing the activation of PI3K/Akt/NF-κB pathway, therefore, reduced the nuclear translocation of phosphorylated NF-κB, leading to the down-regulation of the gene expressions of TNF-α, i NOS and IL-1β and thus lessened the production of i NOS, TNF-α and COX-2 protein. |
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