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 CCl