Objective To investigate the possible mechanisms of Langchuangding in the treatment of liver and kidney yin deficiency syndrome in active stage of systemic lupus erythematosus（SLE）. Methods Patients with liver and kidney yin deficiency syndrome and normal subject whole blood peripheral blood mononuclear cell（PBMC） of active SLE were collected and divided into a model group

a Langchuangding group（Langchuangding freeze-dry powder 2μg/μl）

a Langchuangding+dexamethasone group（Langchuangding freeze-dry powder 2μg/μl + dexamethasone injection 10μg/ml）

and a dexamethasone group（dexamethasone injection 10μg/ml）. Cells were collected 24 hours after drug administration and flow cytometry was used to detect plasmacytoid dendritic cells（pDC） content in normal and active SLE patients and PBMC in each group. Levels of toll-like receptor 7（TLR7）

toll-like receptor 9（TLR9） and myeloid differentiation factor 88（MyD88） mRNA expression in PBMC cells in each group were detected by Realtime-PCR. Protein expression levels of TLR7

TLR9

MyD88 and nuclear factor-κB p65（NF-κB p65） were detected by Western blotting

and the content of IFN-α in the supernatant was detected by ELISA. Results Compared with normal subjects

pDC content in peripheral blood PBMC of active SLE patients decreased（P<0.01）. Compared with the model group

pDC content

NF-κB p65 protein expression increased

MyD88 mRNA and TLR7 and TLR9 protein expression decreased

and IFN-α content in culture supernatant decreased in the Langchuangding group（P<0.05 or P<0.01）. TLR9

MyD88 mRNA and TLR9

MyD88

NF-κB p65 protein and IFN-α content in culture supernatant was decreased Langchuangding + dexamethasone group（P<0.05 or P<0.01）. Compared with dexamethasone group

the content of pDC in Langchuangding group increased

the expression of TLR7 and MyD88 mRNA decreased

and the content of IFN-α in culture supernatant decreased. Expression of TLR7

TLR9

MyD88 mRNA and MyD88

NF-κB p65 protein and IFN-α content in culture supernatant in Langchuangding+dexamethasone group decreased（P<0.01）. Compared with Langchuangding group

the expression of NF-κB p65 protein in Langchuangding + dexamethasone group was decreased（P<0.01）. Conclusion Langchuangding and the combination of Langchuangding and dexamethasone may inhibit the TLR7/TLR9/MyD88 signaling pathway of PBMC in active SLE patients by increasing pDC content in PBMC

thus inhibiting the progression of SLE

and the effects of Langchuangding combined with dexamethasone is supperior.