To investigate the mechanism of Sanqi (Notoginseng Radix et Rhizoma) improving the renal fibrosis induced by adriamycin in rats with blood stasis syndrome based on proteomics.

Thirty SD rats were randomly divided into 6 groups: normal group, model group, Sanqi (Notoginseng Radix et Rhizoma) low-dose group, Sanqi (Notoginseng Radix et Rhizoma) medium-dose group, Sanqi (Notoginseng Radix et Rhizoma) high-dose group and positive control group, with 5 rats in each group. Using LC-MS technology in combination with bioinformatics analysis, protein identification, quantification and differential protein screening were performed on renal tissues. Differential proteins were subjected to GO and KEGG enrichment analysis.

There were 478 proteins in the model group compared with those in the normal group, of which 146 proteins were up-regulated and 332 proteins were down-regulated. Compared with those in the model group, there were 180 different proteins in the Sanqi (Notoginseng Radix et Rhizoma) medium-dose group, including 76 up-regulated and 104 down-regulated proteins. Combined with the above experimental results, further analysis of the Sanqi (Notoginseng Radix et Rhizoma) medium-dose group, the model group and the normal group showed that there were 7 differentially expressed proteins regulated by Sanqi (Notoginseng Radix et Rhizoma) . Among them, the proteins that Sanqi (Notoginseng Radix et Rhizoma) may up-regulate were Gtf2f2 and LOC681410. The possible down-regulated proteins were RT1-Ba, Cnpy4, Pdcd11, Gimap4 and P3h1. KEGG pathway enrichment results showed that the most significant energy pathway was metabolic pathways.

Sanqi (Notoginseng Radix et Rhizoma) may play a role in anti-renal fibrosis in adriamycin-induced rat model with blood stasis syndrome through multi-target and multi-pathway by regulating differential expressions of renal tissue proteins Gtf2f2, LOC681410, RT1-Ba, Cnpy4, Pdcd11, Gimap4 and P3h1 and modulating metabolic pathways associated with energy metabolism.