Figure 5
From: Establishment of Novel Murine Model showing Vascular Inflammation-derived Cognitive Dysfunction
Vascular inflammation induced by abdominal aortic aneurysm accelerates cognitive dysfunction in senescence-accelerated mice prone 8 (SAMP8). (A–D) Morris water maze test in senescence-accelerated mice resistant 1 (SAMR1) and SAMP8 4 weeks after sham operation (Sham) or angiotensin II (AngII) infusion with calcium chloride (CaCl2) application (CaCl2 + AngII). (A) SAMP8 after CaCl2 + AngII showed significant impairment of escape latency in the hidden platform trial. (B,C) Swim time spent (B) and number of platform crossings (C) in target quadrant (TQ) vs. other quadrants (OQs). Values of the three OQs were combined and averaged. (D) Representative searching strategy in the probe test. (E) Slope of fEPSP significantly decreased in SAMP8 after CaCl2 + AngII. (F) Representative aorta and histopathological analysis of infrarenal aorta in SAMR1 and SAMP8 after sham operation (Sham) or AngII infusion with CaCl2 application (CaCl2 + AngII). (G) Immunofluorescent staining for macrophages (green: Mac3, blue: DAPI) and EVG staining. (H) There was an inverse correlation between infrarenal aortic diameter and quadrant time in the probe trial. *p < 0.05, **p < 0.01, ***p < 0.001. Scale bar = 100 µm. n = 6 for SAMR1 [Sham], n = 5 for SAMR1 [CaCl2 + AngII], n = 6 for SAMP8 [Sham] and n = 4 for SAMP8 [CaCl2 + AngII] (A–D); n = 15 for SAMR1 [Sham], n = 12 for SAMR1 [CaCl2 + AngII], n = 13 for SAMP8 [Sham] and n = 10 for SAMP8 [CaCl2 + AngII] (E).
