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Objective: To investigate the antiproliferative and apoptogenic activities of polysaccharides extracted from Dioscorea bulbifera L (DBP) and Chinese Angelica (CAP) and a 3:2 mixture of these compounds (DCCP) on two esophageal carcinoma cell lines, EC9706 and Eca109. Methods: A MTT assay was used to detect the effects of DBP (10 μg/ml and 100 μg/ml), DCCP(17 μg/ml and 170 μg/ ml) and CAP (10 μg/ml and 100 μg/ml) on the proliferation of EC9706 and Eca109 cells. DNA content analysis by flow cytometry was used to determine the cell cycle distribution, and Annexin V-FITC/PI stained fluorescence-activated cell sorter (FACS) was used to detect the apotosis rate of treated cells. Western blots were used to examine protein levels. Results: DBP and DCCP strongly inhibited the proliferation and viability of both the EC9706 and Eca109 cells. CAP enhanced the effects of DBP. DCCP primarily arrested the EC9706 and Eca109 cells at the G1 phase of the cell cycle. DCCP induced apoptosis in both esophageal carcinoma cell lines, and reduced the expression of pIκBα and Bcl-2 proteins. Conclusion: DCCP triggered apoptosis in esophageal carcinoma cells by inhibiting the NF-κB signaling pathway.
Objective: To investigate the antiproliferative and apoptogenic activities of polysaccharides extracted from Dioscorea bulbifera L (DBP) and Chinese Angelica (CAP) and a 3: 2 mixture of these compounds (DCCP) on two esophageal carcinoma cell lines, EC9706 and Eca 109. Methods: A MTT assay was used to detect the effects of DBP (10 μg / ml and 100 μg / ml), DCCP (17 μg / ml and 170 μg / ml) and CAP (10 μg / ml and 100 μg / ml) on the proliferation of EC9706 and Eca109 cells. DNA content analysis by flow cytometry was used to determine the cell cycle distribution, and Annexin V-FITC / PI stained fluorescence-activated cell sorter (FACS) was used to detect the apotosis rate of treated cells. Western Results: DBP and DCCP strongly inhibited the proliferation and viability of both the EC9706 and Eca109 cells. CAP enhanced the effects of DBP. DCCPs arrested the EC9706 and Eca109 cells at the G1 phase of the cell cycle DCCP induced apoptosis in both e sophageal carcinoma cell lines, and reduced the expression of pIκBα and Bcl-2 proteins. Conclusion: DCCP triggered apoptosis in esophageal carcinoma cells by inhibiting the NF-κB signaling pathway.