Figure 3.

The Keap1/Nrf2 signaling pathway mediates the pathogenesis and progression of T1DM in mice. (a) A stimulated T1DM animal model in Nrf2^−/− C57BL/6J mice was established by injection with ALX (60 mg/kg body weight) via the tail vein after 24 hours of fasting. The fasting blood glucose concentrations and body weights were measured every three days for one month. (b) Average blood glucose concentration curves for the mice. (c) Average body weight curves for the mice. (d) Organ indexes for mouse livers, hearts, spleens, lungs, kidneys, and thymuses. (e) Representative images showing hematoxylin and eosin staining of pancreatic islets for the mice. (f) The insulin concentrations in mouse plasma were assessed by using an ELISA Kit. (g) The insulin in the pancreatic islets of the mice was detected by immunohistochemistry. (h) The insulin and glucagon in the pancreatic islets of the mice were detected by immunofluorescence. Comparison of the blood glucose concentrations (i), insulin (j), and glucose levels (k) between the WT and Nrf2^−/− mice exposed to the same ALX treatment. The data represent the mean ± SD (n = 5). ^∗∗p < 0.01 and ^∗∗∗p < 0.001 compared with the control group for (b)–(g); ^∗∗∗p < 0.001 compared with the WT group for (i)–(k).