Artemisia capillaris (A. capillaries) is known to play roles in many cellular events, such as cellproliferation, differentiation, and apoptosis. We investigated the antifibrogenic efficacy of A.capillaris in the immortalized human hepatic stellate cell line LX2. Cell proliferation wasdetermined by the MTT assay. Cell cycle was analyzed by the flow cytometry. Apoptotic cellswere measured using a cell death detection ELISA. Caspase activity was detected by acolorimetric assay. The mRNA level of Bcl-2 and Bax mRNA were measured by real-time PCR.MEK and ERK protein were detected by Western blot analysis. We provide evidence that A.capillaris induces cell cycle arrest, apoptosis, and potently inhibits the mitogen-activatedprotein kinase pathway. A. capillaris inhibited cell proliferation of LX2 cells in a dose- andtime-dependent manner, increased the apoptosis fraction at cell cycle analysis with anaccompanying DNA fragmentation, and resulted in a significant decrease in Bcl-2 mRNA levelsand an increase in Bax expression. Exposure of LX2 cells to A. capillaris induced caspase-3activation, but co-treatment of A. capillaris with the pan-caspase inhibitor Z-VAD-FMK, andthe caspase-3 inhibitor Z-DEVE-FMK, blocked apoptosis. A. capillaris down-regulated Mcl-1protein levels and inhibited phosphorylation of MEK/ERK, suggesting that it mediates celldeath in LX2 cells through the down-regulation of Mcl-1 protein via a MEK/ERK-independentpathway.