Objective To investigate the molecular mechanism of rosmarinic acid (RA) in the treatment of liver fibrosis. Methods HSC-T6 cells were divided to control group, TGF-β1 group, TGF-β1+RA150 μM group, TGF-β1+RA200 μM group and TGF-β1+RA250 μM group. The effect of rosmarinic acid on the activity of HSC-T6 cells was measured using CCK-8. ELISA was used to measure the levels of α-smooth muscle actin (α-SMA), Collagen Ⅰ (COL-Ⅰ), NOD-like receptor protein 3(NLRP3), thioredoxin-interacting protein(TXNIP), IL-1β, and IL-18. q-PCR and Western blotting were performed to detect the expression of the TXNIP/NLRP3/Caspase-1 pathway.Results RA showed an inhibitory effect on HSC-T6 cells compared with the control group (P＜0.05). Compared with TGF-β1 group, RA treatment reduced the levels of α-SMA, COL-Ⅰ, TXNIP, NLRP3, IL-1β, and IL-18 in HSC-T6 cells compared to the TGF-β1 stimulation group (P＜0.05), and downregulated the mRNA and protein expressions of the TXNIP/NLRP3/Caspase-1 pathway.Conclusion RA has an inhibitory effect on HSC-T6 cells. This effect may be regulated to the regulation of the TXNIP/NLRP3/Caspase-1 inflammasome signaling pathway and the inhibition of inflammatory factor release, which ultimately inhibits the growth of HSCs