Figure 4.

SAA-induced increase in the oxidative damage marker F2-isoporstane in aortae can be prevented by preloading with HDL. Male ApoE⁻/⁻ mice were randomly allocated into 4 treatment arms and administered with vehicle (control), LPS, SAA alone, or SAA in combination with HDL. Mice were monitored for 4 weeks (young group, panel A) or 18 weeks (old group, panel B) after commencement of treatment then sacrificed and aortae harvested. Clarified tissue homogenates were prepared and analyzed for free (unesterified) F₂-isoprostane content per protein level by ELISA, as described in the methods sections. Each aortic homogenate obtained from control (n = 8), LPS (n = 8), SAA (n = 8), and HDL/SAA (n = 8) mice was sampled twice, and the output averaged from these 2 replicate measurements of oxidized lipid and then expressed as mean ± SD for each mouse cohort. ** Different to control and LPS group, p < 0.01. ^## Different to SAA and HDL-SAA group, p < 0.01.