Effects of NF-κB Inhibitor on Cisplatin-induced Apoptosis in Cervical Cancer

Objective To observe whether cisplatin-induced apoptosis were increased when SiHa cells were preincubated with nuclear factor-kappa B (NF-κB) inhibitorsaspirin, sulindac, curcumin or pyrrolidine dithiocarbamate (PDTC). Methods SiHa cells were preincubated 2 hours with aspirin, sulindac, curcumin and PDTC respectively, then a further incubation were done with cisplatin, and Western blot analysis were applied to detect P65 level of nuclear extraction. MTT assay was done to detect relative cell viability. TUNEL was applied to detect apoptosis rates. Flow cytometryies with PI staining were also used to detect apoptosis as well as cell cycle. Results When SiHa cells were pretreated with aspirin, sulindac, curcumin or PDTC, Western blot showed that the expression of P65 was inhibited upon cisplatin stimulus (P<0.05). MTT assay demonstrated that a preincubation with NF-κB inhibitor could signifianctly increase cisplatin-induced chemosensitivity (P<0.05). When cells pretreated with aspirin, sulindac, curcumin, or PDTC, TUNEL and flow cytometries assay showed that the apoptotic rates were all increased after 24 hours cisplatin stimulus (P<0.05). Results of flow cytometries were also showed that a pretreation with aspirin, sulindac, curcumin, or PDTC could significantly increase cisplatin-induced apoptosis. Conclusion Aspirin, sulindac, curcumin and PDTC could all inhibit cisplatin induced NF-κB activiation, which could increase cispaltin-induced chemosensativity by augments of apoptosis.