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Key molecular mechanisms of ACs anti-inflammatory activity are generally through NF-B inhibition, where AC inhibits the phosphorylation and degradation of IB-, thus preventing the nuclear translocation of NF-B p65

A3D8 inhibited the proliferation of HL-60 cells, and its differentiation mechanism was associated with the up-regulation of p21 cip1 expression and downregulation of cyclin D1 and CDK4 expression (106)

Cells from each group were harvested, washed with cold PBS, and resuspended in 1 binding buffer at a concentration of 1 10 6 cells/mL

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