2014Tianjin yiyaoRequires access

Inhibitory Effects of Oridonin Combined with Gemcitabine on Pancreatic Cancer SW1990 Cells

Limin Zhou

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Abstract

Objective cancer SW1990 cells in vitro, and the potential mechanisms thereof. Methods The pancreatic cancer SW1990 cells weretreated with vehicle alone and various concentrations(10,20,40,80 and160 μmol/L) of oridonin, followed by 24, 48 and 72 hcell culture. Effects of oridonin on cell proliferation were determined by using a CCK-8 kit. SW1990 cells were treated withoridonin(40 μmol/L) and gemcitabine(20 μmol/L) alone or together for 48 h, and the untreated cells were used as the con-trol. The cell survival rate was detected by CCK-8 assay. Apoptosis induction was assessed by using Annexin V-FITC kit.Semi-quantitative RT-PCR was used to examine the changes of NF-κB mRNA and XIAP mRNA expressions. ResultsOridonin inhibited the growth of pancreatic cancer SW1990 cells in a dose- and time-dependent manner. Compared withthe other groups, the cell survival rate was significantly lower in the combination group(P 0.05). Oridonin combined withgemcitabine induced a higher percentage of apoptosis in pancreatic cancer cells than that of oridonin or gemcitabine alone(P 0.05). Moreover, the expressions of NF-κB and XIAP mRNA in pancreatic carcinoma cells were obviously down-regu-lated in combination group(P 0.05). Conclusion Oridonin can enhance the antitumor effect of gemcitabine on pancreaticcancer in vitro, which may be related to through the down-regulation of NF-κB and its downstream of XIAP, and then induc-ing cell apoptosis in pancreatic cancer.

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Objective cancer SW1990 cells in vitro, and the potential mechanisms thereof. Methods The pancreatic cancer SW1990 cells weretreated with vehicle alone and various concentrations(10,20,40,80 and160 μmol/L) of oridonin, followed by 24, 48 and 72 hcell culture. Effects of oridonin on cell proliferation were determined by using a CCK-8 kit. SW1990 cells were treated withoridonin(40 μmol/L) and gemcitabine(20 μmol/L) alone or together for 48 h, and the untreated cells were used as the con-trol. The cell survival rate was detected by CCK-8 assay. Apoptosis induction was assessed by using Annexin V-FITC kit.Semi-quantitative RT-PCR was used to examine the changes of NF-κB mRNA and XIAP mRNA expressions. ResultsOridonin inhibited the growth of pancreatic cancer SW1990 cells in a dose- and time-dependent manner. Compared withthe other groups, the cell survival rate was significantly lower in the combination group(P 0.05). Oridonin combined withgemcitabine induced a higher percentage of apoptosis in pancreatic cancer cells than that of oridonin or gemcitabine alone(P 0.05). Moreover, the expressions of NF-κB and XIAP mRNA in pancreatic carcinoma cells were obviously down-regu-lated in combination group(P 0.05). Conclusion Oridonin can enhance the antitumor effect of gemcitabine on pancreaticcancer in vitro, which may be related to through the down-regulation of NF-κB and its downstream of XIAP, and then induc-ing cell apoptosis in pancreatic cancer.

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Available abstract

Objective cancer SW1990 cells in vitro, and the potential mechanisms thereof. Methods The pancreatic cancer SW1990 cells weretreated with vehicle alone and various concentrations(10,20,40,80 and160 μmol/L) of oridonin, followed by 24, 48 and 72 hcell culture. Effects of oridonin on cell proliferation were determined by using a CCK-8 kit. SW1990 cells were treated withoridonin(40 μmol/L) and gemcitabine(20 μmol/L) alone or together for 48 h, and the untreated cells were used as the con-trol. The cell survival rate was detected by CCK-8 assay. Apoptosis induction was assessed by using Annexin V-FITC kit.Semi-quantitative RT-PCR was used to examine the changes of NF-κB mRNA and XIAP mRNA expressions. ResultsOridonin inhibited the growth of pancreatic cancer SW1990 cells in a dose- and time-dependent manner. Compared withthe other groups, the cell survival rate was significantly lower in the combination group(P 0.05). Oridonin combined withgemcitabine induced a higher percentage of apoptosis in pancreatic cancer cells than that of oridonin or gemcitabine alone(P 0.05). Moreover, the expressions of NF-κB and XIAP mRNA in pancreatic carcinoma cells were obviously down-regu-lated in combination group(P 0.05). Conclusion Oridonin can enhance the antitumor effect of gemcitabine on pancreaticcancer in vitro, which may be related to through the down-regulation of NF-κB and its downstream of XIAP, and then induc-ing cell apoptosis in pancreatic cancer.

Key concepts: Gemcitabine, XIAP, Pancreatic cancer, Apoptosis, Annexin, In vitro, Cancer research, Cell culture

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