An Liu1, Jiang Luo, Jian-Hong Zhang. 1. Surgery Department of Second Affiliated Hospital of Wenzhou Medical College, Zhejiang 325027.
Abstract
OBJECTIVE: To study the effect of emodin combined gemcitabine on the growth of pancreatic cancer in vivo and in vitro as well as its mechanisms. METHODS: After human pancreatic cancer cell line SW1990 was treated with emodin (40 micromol/L), gemcitabine (20 micromol/L), and emodin combined gemcitabine, the cell proliferation was detected by cell counting kit-8 (CCK-8) assay. The apoptosis of pancreatic cancer cells was detected using the flow cytometry (FCM). The protein expressions of Bax and Bcl-2 were detected using Western blot. SW1990 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors. The mice were then treated by emodin, gemcitabine, and emodin combined gemcitabine, respectively. The changes of tumor volume were monitored. The positive expressions of Ki-67, Bax, and Bcl-2 in the xenograft tumors were detected using immunohistochemical method. RESULTS: Emodin combined with gemcitabine induced a higher percentage of growth inhibition and apoptosis in pancreatic cancer cell line SW1990 than that of gemcitabine or emodin alone (P < 0.05). The protein expression of Bax was up-regulated and that of Bcl-2 down-regulated in the emodin group and the emodin combined gemcitabine group when compared with the control group (P < 0.05). Emodin combined with gemcitabine could significantly inhibit the growth of pancreatic xenograft tumors, increase the positive expression of Bax in tumor tissues, obviously decrease the positive expressions of Ki-67 and Bcl-2 (P < 0.05). The optimal effects were obtained in the emodin combined gemcitabine group (P < 0.05). CONCLUSION: Emodin could potentiate the inhibition of pancreatic cancer growth induced by gemcitabine both in vitro and in vivo, which might be achieved by up-regulating the expression of Bax and down-regulating the expression of Bcl-2.
OBJECTIVE: To study the effect of emodin combined gemcitabine on the growth of pancreatic cancer in vivo and in vitro as well as its mechanisms. METHODS: After humanpancreatic cancer cell line SW1990 was treated with emodin (40 micromol/L), gemcitabine (20 micromol/L), and emodin combined gemcitabine, the cell proliferation was detected by cell counting kit-8 (CCK-8) assay. The apoptosis of pancreatic cancer cells was detected using the flow cytometry (FCM). The protein expressions of Bax and Bcl-2 were detected using Western blot. SW1990 cells were injected subcutaneously into nude mice to establish pancreatic xenograft tumors. The mice were then treated by emodin, gemcitabine, and emodin combined gemcitabine, respectively. The changes of tumor volume were monitored. The positive expressions of Ki-67, Bax, and Bcl-2 in the xenograft tumors were detected using immunohistochemical method. RESULTS:Emodin combined with gemcitabine induced a higher percentage of growth inhibition and apoptosis in pancreatic cancer cell line SW1990 than that of gemcitabine or emodin alone (P < 0.05). The protein expression of Bax was up-regulated and that of Bcl-2 down-regulated in the emodin group and the emodin combined gemcitabine group when compared with the control group (P < 0.05). Emodin combined with gemcitabine could significantly inhibit the growth of pancreatic xenograft tumors, increase the positive expression of Bax in tumor tissues, obviously decrease the positive expressions of Ki-67 and Bcl-2 (P < 0.05). The optimal effects were obtained in the emodin combined gemcitabine group (P < 0.05). CONCLUSION:Emodin could potentiate the inhibition of pancreatic cancer growth induced by gemcitabine both in vitro and in vivo, which might be achieved by up-regulating the expression of Bax and down-regulating the expression of Bcl-2.