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AIM:To investigate the effect of propofol on human pancreatic cells and the molecular mechanism of propofol action.METHODS:We used the human pancreatic cancer cell line MIAPaCa-2 for in vitro studies measuring growth inhibition and degree of apoptotic cell death induced by propofol alone,gemcitabine alone,or propofol followed by gemcitabine.All experiments were conducted in triplicate and carried out on three or more separate occasions.Data were means of the three or more independent experiments±SE.Statistically significant differences were determined by two-tailed unpaired Student’s t test and defined as P<0.05.RESULTS:Pretreatment of cells with propofol for 24 h followed by gemcitabine resulted in 24%-75% growth inhibition compared with 6%-18%when gemcitabine was used alone.Overall growth inhibition was directly correlated with apoptotic cell death.We also showed that propofol potentiated gemcitabine-induced killing by downregulation of nuclear factor-κB(NF-κB).In contrast,NF-κB was upregulated when pancreatic cancer cells were exposed to gemcitabine alone,suggesting a potential mechanism of acquired chemoresistance.CONCLUSION:Inactivation of the NF-κB signaling pathway by propofol might abrogate gemcitabineinduced activation of NF-κB,resulting in chemosensitization of pancreatic tumors to gemcitabine.
AIM: To investigate the effect of propofol on human pancreatic cells and the molecular mechanism of propofol action. METHODS: We used the human pancreatic cancer cell line MIAPaCa-2 for in vitro studies measuring growth inhibition and degree of apoptotic cell death induced by propofol alone , gemcitabine alone, or propofol followed tripled and carried out on three or more separate occasions. Data were means of the three or more independent experiments ± SE. Statistically significant differences were determined by two-tailed unpaired Student’s t test and defined as P <0.05.RESULTS: Pretreatment of cells with propofol for 24 h followed by gemcitabine resulted in 24% -75% growth inhibition compared with 6% -18% when gemcitabine was used alone. with apoptotic cell death. We also showed that propofol potentiated gemcitabine-induced killing by downregulation of nuclear factor-κB (NF-κB) .In contrast, NF-κ B was upregulated when pancreatic cancer cells were exposed to gemcitabine alone, suggesting a potential mechanism of acquired chemoresistance. CONCLUSION: Inactivation of the NF-κB signaling pathway by propofol might abrogate gemcitabine induced activation of NF-κB, resulting in chemosensitization of pancreatic tumors to gemcitabine .