Fig. 7

Blocking the NF-κB–HIF-1α–CXCL1 signaling axis reduces neutrophil infiltration and improves AP. A H&E staining, edema degree score, and inflammation score of pancreatic tissues of mice in normal control group, AP group, and AP + SC75741 (NF-κB inhibitor) group. B Western blot diagrams of P65, pP65, and CXCL1 in pancreatic tissues of normal control group, AP group, and SC75741 + AP group. C Immunohistochemical diagram of CXCL1 in pancreatic tissues of normal control group, AP group, and SC75741 + AP group. D Percentage of neutrophils and immunofluorescence diagram of NETs in pancreatic tissues of normal control group, AP group, and SC75741 + AP group (MPO, red, neutrophil marker; CITH3, green; yellow image is NETs). F Diagram showing animal experiment operation. G H&E staining, edema degree score, and inflammation score of pancreatic tissues of mice in normal control group, AP group, AP + PX-478 (HIF-1α inhibitor) group, and AP + SRT3109 (CXCR2 antagonist) group. H Levels of serum amylase and lipase in mice in normal control group, AP group, AP + PX-478 (HIF-1α inhibitor) group, and AP + SRT3109 (CXCR2 antagonist) group. I mRNA expression levels of inflammatory factors in each group. J Western blot diagrams of P65, pP65, and CXCL1 in each tissue. K Immunohistochemical diagrams of CXCL1 in each group. L Percentage of neutrophils and immunofluorescence diagram of NETs in pancreatic tissues of each group (MPO, red, neutrophil marker; CITH3, green; yellow image is NETs). Student’s t-test was used for comparison between two groups. *P < 0.05 is considered statistically significant, **P < 0.01, ***P < 0.001