LAUSR

&NA; According to conservative estimates, >230 million people are infected with schistosomiasis,which becomes one of the most common parasitic diseases. This study focuses on investigating in vivo and in vitro effects of mmu‐miR‐92a‐2‐5p in Schistosoma japonicum‐induced liver fibrosis by targeting TLR2. Through bioinformatic analysis, the overexpression of TLR2 and the down‐regulation of mmu‐miR‐92a‐2‐5p were revealed in the progression of S. japonicum‐induced liver fibrosis. BALB/C mice were taken advantage to construct normal control and schistosomiasis liver fibrosis (SLF) model. The mice in model groups were transfected recombinant lentivirus (Lenti‐mmu‐miR‐92a‐2‐5p or Lenti‐NC) to alter the expression of mmu‐miR‐92a‐2‐5p in vivo. HE and Masson staining were employed to observe the pathological changes and collagenous fibrosis. QRT‐PCR showed that mmu‐miR‐92a‐2‐5p was decreased while TLR2 was elevated in the infected groups. However, lenti‐mmu‐miR‐92a‐2‐5p group could inhibit liver fibrosis. Then the effect of mmu‐miR‐92a‐2‐5p on S. japonicum‐induced liver fibrosis including cell apoptosis rates, proliferation and proteins related to liver fibrosis was examined in NIH‐3T3 mouse embryonic fibroblasts. Moreover, the association between mmu‐miR‐92a‐2‐5p and TLR2 was detected by dual‐luciferase reporter gene assay and the expression of cytokines IL‐4, IFN‐&ggr; and TNF‐&agr; in SLF model was detected by ELISA. Further, the knockout of TLR2 in C57BL/6J mice was used to confirm the association between mmu‐miR‐92a‐2‐5p and TLR2. Thus, these findings demonstrated that mmu‐miR‐92a‐2‐5p inhibited S. japonicum‐induced liver fibrosis by targeting TLR2 in vitro and in vivo.