Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway

Figure 5 Inhibition of tumor necrosis factor-α expression reversed the alterations in the Bax/Bcl-2/caspase-3 apoptotic signaling pathway in acute pancreatitis models. A: Western blot analysis of caspase-3, Bcl-2, and Bax expression in MIN-6 cells under control conditions, lipopolysaccharide stimulation (10 μg/mL), and co-culture with media from 266-6 cells, with or without tumor necrosis factor-α inhibitor treatment; B-D: Quantitative analysis of Bcl-2, Bax and caspase-3 relative protein expression in vitro acute pancreatitis model. Representative results from three independent replicate assays are shown. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001. Data are presented as the mean ± SD. LPS: Lipopolysaccharide.