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. 2011 Feb 14;46(3):193–204. doi: 10.1530/JME-10-0117

Figure 6.

Figure 6

Effects of 24 h exposure to cytokines on β-cell death and NF-κB pathway in islets from UCP2+/+ and UCP2−/− mice. In all cases, n=4. Basal=untreated control islets, cytokines=IL1β+IFNγ+TNF-α. (A) Cytokine-induced apoptosis, as percentage of total β-cells from UCP2+/+ and UCP2−/− islets after 24 h exposure. Effects of concurrent BAY 11-7082 (10 μM) are shown. The iNOS inhibitor 1400W (10 μM, 24 h) inhibited apoptosis induced by cytokines to 8·4±0·7% in UCP2+/+ and 5·8±0·9% in UCP2−/− islets (P<0·05 for both). (B) Effects of 24 h cytokines on NF-κB activation in UCP2+/+ and UCP2−/− islets in cytokine-treated cells and those incubated concurrently with inhibitors. The IKKβ inhibitor BAY strongly inhibited NF-κB activation in UCP2+/+ but not in UCP2−/− islets. The iNOS inhibitor 1400W inhibited NF-κB transactivation in both UCP2+/+ and UCP2−/− islets (P<0·05 for both). CAPE also inhibited NF-κB transactivation in both UCP2+/+ and UCP2−/− islets (P<0·05 for both). (C) Phosphorylation of IκBα basally or stimulated by cytokines in the presence and absence of BAY in UCP2+/+ and UCP2−/− islets. (D) Expression of IKKβ mRNA in control and cytokine-treated islets. *P<0·05, effect of cytokines; §P<0·05 for genotype effect; #P<0·05, effect of cytokines compared with basal).