Fig. 1

Disruption of myeloid-specific Notch1 aggravates IR-induced liver injury and increases macrophage accumulation and proinflammatory mediators in IR-stressed liver. The Notch1^FL/FL, Notch1^M−KO and WT mice were subjected to 90 min of partial liver warm ischemia, followed by 6 h of reperfusion. A The nuclear NICD expression was detected in liver macrophage cells from IR-stressed livers by Western blot assay. Representative of three experiments. B Representative histological staining (H&E) of ischemic liver tissue (n = 4–6 mice/group) and Suzuki’s histological score. Scale bars, 200 μm. C Liver function in serum samples was evaluated by serum ALT levels (IU/L) (n = 4–6 samples/group). D Immunohistochemistry staining of CD11b⁺ macrophages in ischemic livers (n = 4–6 mice/group). Quantification of CD11b⁺ macrophages, Scale bars, 40 μm. E Quantitative RT-PCR analysis of TNF-α, IL-1β, CCL-2 and CXCL-10 mRNA levels in ischemic livers (n = 3–4 samples/group). All data represent the mean ± SD. *p < 0.05. **p < 0.01