Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

Figure 1

NLRP3 knockout improves the abnormal response to glucose in mice administration of AGEs. C57BL/6J (WT) and NLRP3 knockout (NLRP3 KO) mice were injected intraperitoneally with 120 mg/kg AGEs or BSA for 6 weeks. (a) Pancreatic sections were stained by insulin (green), glucagon (red), and DAPI (blue), with representative islets shown (scale bar = 50 μm). Histogram represents quantitative analysis of insulin-positive beta cell area (b) and glucagon-positive alpha cell area (c) in each experimental group. per group. Fasting glucose (d) and insulin (e) as well as insulin tolerance (f) were not obviously changed in each group. GTT (d) and IRT (e) were performed after intraperitoneal injection of glucose (1.5 mg/g). per group. Ablation of NLRP3 improved the abnormal glucose metabolism induced by AGE injection. Values are expressed as mean ± SD, ^# versus WT + BSA group. versus WT + AGEs group.

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