Objective: To investigate the stimulatory effect of epinephrine(Epi) and the antagonistic effect of Chrysanthemum indicum Linné extracts (CILE) on Epi-induced growth of human hepatocellular carcinoma(HCC) cells. Methods: The stimulatory effect of Epi and inhibitory effect of CILE on the growth of HepG2 and MHCC97H cells were investigated using a proliferation assay in correlation with βadrenergic receptor(β 2-AR) blockade, a MEK1/MEK2 inhibitor, and assessment of MAPK/ERK1/2 intracellular activity. Results: Epi transiently activated MAPK/ERK1/2 in HepG2 and MHCC97H cells, resulting in a burst of growth. The effect of Epi was significantly attenuated by ICI 118551 and U0126. CILE exhibited a dose-dependent attenuation of the stimulatory effect of Epi on the growth of both cell lines and inhibited the Epi-induced activation of MAPK/ERK1/2. Conclusion: Epi, mimicking a mitogen, stimulated the growth of HepG2 and MHCC97H cells, and CILE was effective in attenuating this effect of Epi on tumor cells by inhibiting the β2-AR-mediated activation of MAPK/ERK1/2. Objective: To investigate the stimulatory effect of epinephrine (Epi) and the antagonistic effect of Chrysanthemum indicum Linné extracts (CILE) on Epi-induced growth of human hepatocellular carcinoma (HCC) cells. Methods: The stimulatory effect of Epi and inhibitory effect of CILE on the growth of HepG2 and MHCC97H cells were investigated using a proliferation assay in correlation with βadrenergic receptor (β 2-AR) blockade, a MEK1 / MEK2 inhibitor, and assessment of MAPK / ERK1 / 2 intracellular activity. / ERK1 / 2 in HepG2 and MHCC97H cells, resulting in a burst of growth. The effect of Epi was significantly attenuated by ICI 118551 and U0126. CILE showed a dose-dependent attenuation of the stimulatory effect of Epi on the growth of both cell lines and inhibited the Epi-induced activation of MAPK / ERK1 / 2. Conclusion: Epi, mimicking a mitogen, stimulated the growth of HepG2 and MHCC97H cells, and CILE was effective in attenuating this effect of Epi on tumor cells by inhibiting the β2-AR-mediated activation of MAPK / ERK1 / 2.