Fig. 5

nCAR/anti381 and CTD-2555A7.2 binding sequence rescued osteoporosis. A ALP and Alizarin Red staining (left) of MC3T3-E1 cells treated with recombinant miR-381-3p inhibitor (compared with MSA), as detected by ALP staining and Alizarin Red staining, and Alp/Runx2 expression levels of MC3T3-E1 cells treated with recombinant miR-381-3p inhibitor, as detected by RT-PCR (right, mean ± S.D., n = 3). MSA: tRNAMet fused Sephadex aptamer. nCAR/anti381: novel recombinant miR-381-3p inhibitor.B ALP and Alizarin Red staining (left), and Alp/Runx2 expression levels (right) of hMSCs treated with recombinant miR-381-3p inhibitor (mean ± S.D., n = 3). C,D Femoral trabecular mineral apposition rate of C57BL/6 mice after OVX and recombinant miR-381-3p inhibitor treatment (mean ± S.D., n = 4). BL (Baseline): sacrifice before RNA treatment. Sham: sham OVX operation group. OVX: OVX group. Mock: transfection reagent control group. MSA: empty recombinant tRNA treated group. nCAR/anti381: novel recombinant miR-381-3p inhibitor treated group. Scale bar: 10μm. E,F Femoral trabecular mineral apposition rate of C57BL/6 mice after OVX and CTD-2555A7.2 binding sequence and recombinant miR-381-3p inhibitor treatment (mean ± S.D., n = 4). bind: CTD-2555A7.2 binding sequence treated group. 381: novel recombinant miR-381-3p inhibitor treated group. CTD+381: CTD-2555A7.2 binding sequence and recombinant miR-381-3p inhibitor combined treated group. Scale bar: 10μm. G Expression levels of miR-381-3p in primary BMSCs of OVX mice treated with CTD-2555A7.2 binding sequence and recombinant miR-381-3p inhibitor, as detected by RT-PCR (mean ± S.D., n = 3).H TCF7 activities of primary BMSCs of OVX mice treated with CTD-2555A7.2 binding sequence and recombinant miR-381-3p inhibitor, as detected by luciferase reporter assay (mean ± S.D., n = 3).*P < 0.05, **P < 0.01, ***P < 0.001