Fig. 6

Exo-181b enhanced M2 polarization by regulating the PRKCD/AKT signaling pathway. a We applied four online prediction tools including TargetScan, miRanda, PicTar and miRDB for the potential targets of miR-181b. In addition, we determined the targets with GO terms related to inflammation response by bioinformatic analysis and the literature. The Venn diagram was used for intersecting the common genes. The prediction sequence of the position of the 3′UTR of PRKCD combined by miR-181b was showed. b The 293T cells were transfected with pRL-CMV reporter vector overexpressing miR‐181b, and negative control (NC) was used as the control vector and the direct inhibition of PRKCD by miR-181b were confirmed by dual-luciferase assay. c, d The protein expression of PRKCD, p-AKT, AKT, and GAPDH was tested by Western blotting and analyzed by Image J. (*p < 0.05). GO gene ontology; 3′UTR: 3′ untranslated region