Duodenal-jejunal bypass improves hypothalamic oxidative stress and inflammation in diabetic rats via glucagon-like peptide 1-mediated Nrf2/HO-1 signaling

Figure 4 Duodenal jejunal bypass inhibits the production of proinflammatory cytokines by blocking the activation of NF-κB signaling in the hypothalamus of type 2 diabetes mellitus rats. A: The quantitative real-time (qRT)-PCR results of NF-κB and p-NF-κB expression; B: The expression levels of NF-κB and p-NF-κB detected by Western blotting; C: The quantitative densitometric analysis of NF-κB and p-NF-κB; D: Flow cytometry results for standards; E: Flow cytometry results for samples; F: Flow cytometry results for the levels of proinflammatory cytokines interleukin (IL)-1β and IL-6; G: The qRT-PCR results of IL-1β and IL-6 expression; H: Expression levels of IL-1β and IL-6 detected by Western blotting; I: The quantitative densitometric analysis of IL-1β and IL-6. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. T2DM: Type 2 diabetes mellitus; DJB: Duodenal jejunal bypass; IL: Interleukin.