Figure 6.

CAIF and miR‐16 inhibited LPS‐induced activation of the NF‐κB signaling pathway and inflammatory response. After transfection, AC16 cells were incubated with 5 µg/ml LPS for 24 h. Both CAIF and miR‐16 significantly inhibited LPS‐induced NF‐κB activation (A), NF‐κB expression (B), NO generation (C), and inducible nitric oxide synthase messenger RNA transcription (D). Both CAIF and miR‐16 inhibited LPS‐elevated CCL2, CXCL1, and IL‐6 expression at the miRNA (E) and protein (F) levels. C, control cells without transfection; CAIF, cardiac autophagy inhibitory factor; CCL2, C‐C motif chemokine 2; CXCL1, growth‐regulated alpha protein; IL, interleukin; LPS, lipopolysaccharide; miR, miRNA; NC, cells transfected with pcDNA3.1, or NC miRNA; NF‐κB, nuclear factor‐κB; NO, nitric oxide. *p < .05