The activation of hepatic stellate cells (HSCs) is a core event in the pathogenesis of liver fibrosis, typically accompanied by the disappearance of lipid droplets (LDs). Reversing the disappearance of HSCs LDs is a strategy to inhibit HSCs activation and alleviate liver fibrosis. Previous studies have shown that nuclear receptor subfamily 1 group d member 1 (NR1D1), as an important component of the biological clock system, is closely related to lipid metabolism. Our previous evidence indicated that Dihydroartemisinin (DHA) can regulate the lipid droplet metabolism of activated HSCs. Moreover, in CCl₄ induced liver fibrosis mice, the liver clock gene NR1D1 is dysregulated. On this basis we explored the potential molecular mechanism of DHA inhibiting liver fibrosis through NR1D1. We found that DHA can inhibit liver fibrosis by restoring activated LDs of HSCs through inhibiting HSCs lipophagy. In summary, our study emphasizes the importance of NR1D1 in liver fibrosis and the potential of DHA to regulate NR1D1 in the treatment of liver fibrosis, providing a new direction for the treatment of liver fibrosis.