Abstract
Research into inflammation during abdominal aortic aneurysm (AAA) formation remains inconclusive. The present study aimed to demonstrate the temporal and spatial distribution of inflammatory cytokines, and to confirm the effect of peroxisome proliferator‑activated receptor γ (PPARγ) on the incidence of AAA formation and the distribution of inflammation in the disease process. Male apolipoprotein E‑/‑ mice were randomly divided into eight groups: Angiotensin II (Ang‑II)‑only 7, 14, 21, 28 and 42 days groups, Ang‑II with rosiglitazone (RGZ) 28 and 42 days groups, and the saline control 42 days group. The early stage was defined as between 7 and 21 days, and the late stage as between 28 and 42 days. Incidences of early rupture and late rupture, aneurysm formation and the maximum diameters of the aorta were recorded. Suprarenal abdominal aortic tissues were collected for histological analysis, and western blotting was performed to reveal the distribution of inflammation. Treatment with Ang‑II caused a significant dilation of the aorta in the late stage; however, this was not observed in the early stage. RGZ reduced the maximum diameters in the late stage. With the pathological process alterations, the inflammatory type shifted. Regarding temporal distribution, the tumor necrosis factor (TNF)‑α expression level was increased over time, and the interleukin (IL)‑10 expression level significantly decreased. When considering the spatial distribution, TNF‑α was expressed dominantly in the aneurysmal body and IL‑10 was dominant in the aneurysmal neck in the late stage. The PPARγ agonist RGZ may reduce the expression of TNF‑α in the late stage and increase the expression level of IL‑10, maintaining the TNF‑α or IL‑10 expression levels at the same levels as in the early stage. Aortic inflammation during AAA formation is dynamic. Protective anti‑inflammatory cytokines are upregulated in the early 'compensatory stage'; however, pro‑inflammatory cytokines are dominant in the late 'decompensatory stage'. PPARγ is likely to continue to upregulate the expression of anti‑inflammatory cytokines, extend the 'compensatory stage', and decelerate the process of AAA development and rupture.