APOE deficiency enhanced JNK-mediated neuroinflammation. (a) SAH promoted JNK phosphorylation (∗P < 0.05, ∗∗P < 0.01, compared to sham, n = 5), while P-JNK level was higher in APOE−/− mice than in WT mice (##P < 0.01). (b) SAH promoted c-JUN phosphorylation (∗∗P < 0.01, compared to sham, n = 5), while P-c-Jun level was higher in APOE−/− mice than in WT mice (##P < 0.01). (c) Immunofluorescence showing higher level of JNK phosphorylation in microglia in APOE−/− mice than in WT mice. (d–f) ELISA showing that SAH promoted cytokine expression including TNF-α, IL-1β, and IL-6 (∗P < 0.05,, compared to sham, n = 5), while the levels of these cytokines were higher in APOE−/− mice than in WT mice (#P < 0.05, ##P < 0.01). Bar = 50 μM.