Research Paper Volume 12, Issue 11 pp 11116—11138
Deoxyelephantopin induces apoptosis via oxidative stress and enhances gemcitabine sensitivity in vitro and in vivo through targeting the NF-κB signaling pathway in pancreatic cancer
Figure 6. DET inhibited the TNF-α and GEM induced NF-κB activity and sensitized the antitumor effect of GEM in vitro. (A) DET inhibited TNF-α-induced NF-κB activity. (B) Quantitative statistics of immunoblotting assays for NF-κB-p65 levels. **P < 0.01 versus CTL. ##P < 0.01 versus TNF-α single treatment group. CTL, control. (C) DET inhibited GEM-induced NF-κB activity. (D) Quantitative statistics of immunoblotting assays for NF-κB-p65 levels. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. CTL, control. (E) Reduction of cell viability after 24 h combined treatment of DET and GEM, and IKK 16 and GEM in BxPC-3/GEM50 cell line. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. &P < 0.05. CTL, control. (F) DET sensitized cells to the inhibitory effects of GEM on cell viability in BxPC-3/GEM100 cell line. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. &P < 0.05. CTL, control. (G) DET enhanced the inhibitory effect of GEM on cell proliferation in GEM-resistant cell lines. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. &P < 0.05, &&P < 0.01. CTL, control. (H, I) DET reinforced the suppression of GEM on the migration and invasion of GEM-resistant BxPC-3 cell lines. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. &P < 0.05, &&P < 0.01. CTL, control. (J, K) DET amplifies the role of GEM in inducing apoptosis in GEM-resistant BxPC-3 cell lines. **P < 0.01 versus CTL. ##P < 0.01 versus GEM single treatment group. &P < 0.05, &&P < 0.01. CTL, control. Magnification, × 200 (H–K). Scale bar, 100 μm (H–K).