Objective: To investigate the effect of astragaloside on the differentiation of bone marrow mesenchymal stem cells into pericytes^ ^^iods: The MSCs were isolated from SD rats (5d-7d) bone marrow by whole bone marrow primary culture method, purified by amplification in vitro, and the fourth and fifth generation were used in this study. The purified cells were divided into three groups: negative control group, incubated in L-DMEM with 15% FBS without drug intervention; positive control group,cultured with TGF-p1 5 ng/mL for 72 hour; Ast group, cultured with 4 滋g/mL Ast for 1 day, 2 day, 3 day, 5 day and 7 day; blocker group,inhibitor ofthe TGF-p1 type I receptor sb431542 being administered prior to Ast exposure,of which samples were collected at 1 day, 2 day, 3 day. Expression levels ofNG2, 琢-SMA were examined by RT-PCR and Western blot. The expression levels of p-Smad2 and Smad2/3 were examined by Western blot. Results: The mRNA and protein expression level of NG2, 琢-SMA was higher in all Ast group. The mRNA and protein expression level of NG2, 琢-SMA was higher in Ast 3d group, compared with the negative control group and the positive control group (p<0.05). The TGF-茁 1/Smad signaling was activated after Ast intervention. The p-Smad2 protein level increased by day 1, reached a maximum at day 3, and then decreased. The protein expression level of p-Smad2 was higher in Ast 3d group,compared with the Ast 0d group (p<0.01). The effect of the astragaloside is blocked by the inhibitor of the TGF-茁 1 type I sb431542 exposure, leading to the down-regulation ofthe mRNA and protein level ofNG2, 琢-SMA. Compared with the Ast group at the same time point, the mRNA and protein expression level of NG2, 琢-SMA reduced significantly in the blocker group at day3 (p<0.001). The signaling pathway was inhibited, as the p-Smad2 protein level decreased. Compared with the Ast 3d group, the protein expression level of p-Smad2 reduced significantly in the sb431542+Ast 3d group (p<0.001). Conclusion: Astragaloside can induce bone marrow mesenchymal stem cells differentiating into pericytes through the TGF-茁1/Smad2 signaling pathway. [ABSTRACT FROM AUTHOR]