Research Paper Volume 13, Issue 4 pp 5164—5184

Figure 8. Endogenous IMD alleviated CaCl₂-induced AAA and Notch1 signaling and M1 polarization. Control, wild type C57 mice with saline incubation; CaCl₂, wild-type C57 mice with CaCl₂ incubation; CaCl₂+IMD-Tg, IMD transgenic mice with CaCl₂ incubation to induce AAA; CaCl₂+IMD ko, IMD-knockout mice with CaCl₂ incubation to induce AAA. (A) Representative photographs of macroscopic features of aneurysms in male C57 mice at the end of 28 days. Scale bar, 5 mm. (B) Incidence of CaCl₂-induced AAA in animals and maximal abdominal aortic diameter of surviving mice at the end of 28 days. The vascular diameter > 50% of the average diameter of the control group was considered AAA. *P<0.05 vs. Control. ^#P<0.05 vs. CaCl₂. (C) Representative HE staining. Scale bar, 200 μm. (D–F) Immunohistochemistry of the protein expression of NICD, hes1 and iNOS in aortas of mice.