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. 2020 Mar 2;32:101486. doi: 10.1016/j.redox.2020.101486

Fig. 1.

Fig. 1

ALDH2−/−- mice exhibit elevated HNE adduction and diminished markers of synaptic and mitochondrial function without appreciable neuronal loss. (A) Schematic representation of the hydrazine reacting with the free aldehyde of HNE-modified proteins and corresponding immunoblots of whole brain lysates of 3 or 6 month old ALDH2−/− mice or WT littermates incubated with the hydrazine. (B) Quantitative analysis of 6 month old WT and ALDH2−/− cortex and hippocampus lysates probed with a HNE antibody measured by optical density. (C and D) Representative immunofluorescent images of 9 month old WT and ALDH2−/− cortex and hippocampus slices stained for NeuN, and quantitative analysis in optical density units. Optical density was measured for the entire image displayed. (E and F) Quantitative immunoblot analysis of 14 month old cortex and hippocampal homogenates of PSD-95 (95 kDa, E) and pCREB (35 kDa, F). (G and H) qRT-PCR analysis of PGC-1α (G) and SOD1 (H) gene expression in 14 month old cortex and hippocampus homogenates. All genes and proteins were normalized to the housekeeping gene, β-actin. Equal protein amounts were loaded in all lanes of immunoblots. Data represent mean ± S.E.M analyzed by one-way ANOVA with Dunnett's or Tukey's multi-comparison analysis from n = 8–10 mice/genotype/age (*P < 0.05, **P < 0.001, ***P < 0.001).