〔Abstract〕 Objective To explore the role and mechanism of miR-146 a in acute pancreatitis. Methods The expression of miR-146 a, interleukin-1 receptor associated kinase 1(IRAK1),inflammatory cytokines interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) was detected by qPCR and ELISA, and the expression of autophagy related molecules LC3 and p62 was detected by Western blot. miR-146 a and IRAK1 were overexpressed to detect the expression changes of IL-6, TNF-α, LC3 and p62. A mutant plasmid at the binding site of IRAK1 3'UTR and through luciferase reporter gene assay. Results The results showed that taurolithocholic acid 3-sulphate(TLCs) inhibited miR-146 a and IRAK1 expression in a concentration-dependent manner, promoted the expression of IL-6, TNF-α and LC3, and inhibited the expression of p62. Overexpression of miR-146 a could block the effect of TLCs to a certain extent. The luciferase reporter gene results showed that miR-146 a directly targeted IRAK1 and negatively regulated it. Conclusion These results suggested that miR-146 a inhibited inflammation and autophagy in TLCs-induced AR42 J cells by targeting IRAK1.