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 2 Tumor necrosis factor-α levels were elevated in acute pancreatitis models. A: Tumor necrosis factor-α levels in conditioned media from MIN-6 cells were quantified by enzyme-linked immunosorbent assay under control conditions, lipopolysaccharide stimulation (5 μg/mL or 10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells; B: Serum tumor necrosis factor-α levels in acute pancreatitis mouse models were quantified using the same methodology. Representative results from three independent replicates are shown. ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001. Data are presented as the mean ± SD. AP: Acute pancreatitis; TNF-α: Tumor necrosis factor-α; LPS: Lipopolysaccharide; MAP: Mild acute pancreatitis; SAP: Severe acute pancreatitis.