Fig. 7

Peritoneal macrophages from diabetic mice demonstrated an inflammatory state that was attenuated by OI treatment. The peritoneal cells from healthy and diabetic mice were collected and were pretreated with 125 μM OI or NT for 2 h, followed by LPS, OI + LPS, or NT treatment (n = 4 mice per group). A Western blot analysis of the phosphorylated and total levels of ERK, p38, and JNK after 0.5-h treatment. B–D The cells and supernatant were collected after 24-h treatment. IL-1β, IL-6, and TNF-α levels were determined by ELISA and corrected with the protein content. E NO generation in the supernatant was measured by the Griess reaction. F Cell lysates underwent western blotting with Nrf2, HO-1, NQO-1, GCLC, GCLM, NLRP3, iNOS, IL-1β, COX2, and α-tubulin antibodies. The internal control was α-tubulin. G PBMCs collected from non-diabetes (CTR) and type 1 diabetic patients were adhered for 3 h, then pretreated with 125 μM  OI or NT for 2 h, followed by LPS, OI + LPS, or NT treatment. After 24-h treatment, IL-1β levels were in the supernatant (n = 9–10 per group). H Peritoneal macrophages were treated with or without LPS and OI for 8 h, then co-cultured with MIN6 cells for another 24 h. The supernatant was collected and GSIS was analyzed. The results are shown as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. I Schematic depicting the regulatory role of OI on macrophage polarization in protection against type 1 diabetes progression