Fig. 10

rDKK3 promoted the switch of microglia from M1 type to M2 type in neuropathic pain rats via Kremen-1 and DVL-1. a–c Western blot and immunofluorescence results showed that rDKK3 ameliorated the up-regulated protein expression level of Iba-1 in the spinal cord and suppressed the activated microglia caused by neuropathic pain, while treatment with Kremen-1 siRNA or DVL-1 siRNA abolished the effect of rDKK3 on microglia activation (^****p < 0.0001 compared with Sham group, ^####p < 0.0001 compared with SNI + Vehicle group, ^&&&&p < 0.0001 compared with SNI + rDKK3 group, n = 6 in each group). d–f Western blot results indicated that treatment with rDKK3 attenuated the increased protein expression level of CD16, CD86 and iNOS in the spinal cord induced by neuropathic pain, while Kremen-1 siRNA or DVL-1 siRNA abolished the effect of rDKK3 on M1 type biomarkers (^**p < 0.01, ^***p < 0.001, ^****p < 0.0001 compared with Sham group, ^##p < 0.01, ^###p < 0.001, ^####p < 0.0001 compared with SNI + Vehicle group, ^&&p < 0.01, ^&&&p < 0.001, ^&&&&p < 0.0001 compared with SNI + rDKK3 group, n = 6 in each group). g–i Western blot results indicated that application with rDKK3 up-regulated the decreased protein expression level of Arg1, CD206 and IL-10 in the spinal cord caused by neuropathic pain, while administration with Kremen-1 siRNA or DVL-1 siRNA attenuated the effect of rDKK3 on M2 type biomarkers ^(**p < 0.01, ^****p < 0.0001 compared with Sham group, ^#p < 0.05, ^####p < 0.0001 compared with SNI + Vehicle group, ^&&p < 0.01, ^&&&&p < 0.0001 compared with SNI + rDKK3 group, n = 6 in each group)