OBJECTIVE: To explore the effect of emodin combined gemcitabine (E&G) on human pancreatic cancer cell line BxPC-3 in vitro. METHODS: BxPC-3 cells were treated with emodin alone in different concentrations (0, 10, 20, 40, 80, and 160 micromol/L, respectively) for 24, 48, and 72 h, and E&G (emodin 40 micromol/L + gemcitabine 20 micromol/L) for 72 h. The inhibition on BxPC-3 cell proliferation was detected by Cell Counting Kit-8 assay and the cell apoptosis of BxPC-3 was determined using flow cytometry. RESULTS: Emodin obviously suppressed the proliferation of BxPC-3 cells in a dose- and time-dependent manner. The survival rates of BxPC-3 cells by 40 micromol/L emodin for 24, 48, and 72 h were 79. 39%, 46. 35%, and 45. 44%, respectively, while the survival rate of BxPC-3 cells acted by 72-h E&G was only 26. 62%, showing significant difference from that by gemcitabine alone (42.78%) and the emodin alone (47.18%). The early apoptotic ratio of BxPC-3 cells induced by 24 h emodin (40 micromol/L) and gemcitabine (20 micromol/L) were 4.70% +/- 1.54% and 11.20% +/- 1.41% respectively, while early apoptotic ratio of BxPC-3 cells induced by E&G was 20.60% +/-3.23%, showing significant difference from that induced by emodin or gemcitabine alone (P<0.05). CONCLUSIONS: Emodin could significantly inhibit BxPC-3 cell growth. It could act synergistically with gemcitabine to inhibit the tumor proliferation of BxPC-3 cells. Its synergistic action was achieved mainly through inducing pancreatic cancer cell apoptosis.
OBJECTIVE: To explore the effect of emodin combined gemcitabine (E&G) on humanpancreatic cancer cell line BxPC-3 in vitro. METHODS: BxPC-3 cells were treated with emodin alone in different concentrations (0, 10, 20, 40, 80, and 160 micromol/L, respectively) for 24, 48, and 72 h, and E&G (emodin 40 micromol/L + gemcitabine 20 micromol/L) for 72 h. The inhibition on BxPC-3 cell proliferation was detected by Cell Counting Kit-8 assay and the cell apoptosis of BxPC-3 was determined using flow cytometry. RESULTS:Emodin obviously suppressed the proliferation of BxPC-3 cells in a dose- and time-dependent manner. The survival rates of BxPC-3 cells by 40 micromol/L emodin for 24, 48, and 72 h were 79. 39%, 46. 35%, and 45. 44%, respectively, while the survival rate of BxPC-3 cells acted by 72-h E&G was only 26. 62%, showing significant difference from that by gemcitabine alone (42.78%) and the emodin alone (47.18%). The early apoptotic ratio of BxPC-3 cells induced by 24 h emodin (40 micromol/L) and gemcitabine (20 micromol/L) were 4.70% +/- 1.54% and 11.20% +/- 1.41% respectively, while early apoptotic ratio of BxPC-3 cells induced by E&G was 20.60% +/-3.23%, showing significant difference from that induced by emodin or gemcitabine alone (P<0.05). CONCLUSIONS:Emodin could significantly inhibit BxPC-3 cell growth. It could act synergistically with gemcitabine to inhibit the tumor proliferation of BxPC-3 cells. Its synergistic action was achieved mainly through inducing pancreatic cancer cell apoptosis.