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 4 Inhibition of tumor necrosis factor-α expression attenuated the impairment of islet β-cell in acute pancreatitis models. A: Tumor necrosis factor-α levels in MIN-6 conditioned media were measured by enzyme-linked immunosorbent assay under control conditions, lipopolysaccharide stimulation (10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells, with or without treatment with a tumor necrosis factor-α inhibitor; B: Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay; C: Quantitative analysis of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive β-cells; D: Insulin secretion by islet β-cells in the acute pancreatitis model was quantified using an enzyme-linked immunosorbent assay kit. 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. AP: Acute pancreatitis; TNF-α: Tumor necrosis factor-α; LPS: Lipopolysaccharide.