摘要
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 β adrenergic receptor（ β2-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 β adrenergic receptor（ β2-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.
