Fig. 2

CS treatment modifies apoE levels in male E3FAD mice. A In vivo study design. EFAD mice were treated with either vehicle control (VC) or CS by daily intraperitoneal (i.p.) injection from 4 to 8 months of age. B–G Cortical proteins were serially extracted in TBS (soluble), 1% TritonX100 (detergent soluble), and formic acid (insoluble) and apoE levels were measured by ELISA. CS treatment modulated apoE levels only in male E3FAD mice. B CS treatment increased soluble (p = 0.0017) and detergent-soluble apoE (p = 0.0028) and decreased insoluble apoE (p = 0.0323) in male E3FAD mice. C ApoE levels were not affected by CS treatment in female E3FAD mice. D CS treatment reduced insoluble apoE levels in male E4FAD mice (p = 0.0234). E CS treatment reduced detergent-soluble apoE levels in female E4FAD mice (p = 0.0108). F There was a reduction with CS treatment in total apoE levels in female E4FAD (p = 0.0397). G ApoE levels graphed as parts of a whole. ApoE distribution across extracts was modified by CS treatment in male E3FAD (p < 0.0001, analyzed by chi-square (and Fisher’s exact test) *: p < 0.0001. H ABCA1 levels quantified by western blot in the detergent fraction. There were no effects of CS treatment. I Representative image of native gels for apoE measured in the soluble fraction. J–L Quantification of larger (high molecular weight, LP), intermediate (intermediate molecular weight, IP), and small (low molecular weight, SM) apoE particles. There was no effect on levels of LP, IP, or SP with CS treatment. Data are expressed as mean ± SEM (n = 8–12), analyzed by t-test, *: p < 0.05 CS vs. VC. All experiments were done in the cortex. All data is from the same cohort of mice; the n’s differ because of study design, technical issues, and outlier tests