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. 2020 Jun 18;12(6):1824. doi: 10.3390/nu12061824

Figure 4.

Figure 4

PCA treatment significantly reduces lipid peroxidation in the ventral horn of the spinal cord in the hSOD1G93A mouse model of ALS. (A,C) Representative images of lumbar spinal cord ventral horns stained for 4-HNE from two littermate groups of wildtype control mice (WT), untreated hSOD1G93A mice (G93A), and hSOD1G93A mice treated orally with 100 mg/kg PCA beginning at disease onset (G93A+PCA). Mice were euthanized at 105 days of age and ventral horns were stained with an antibody to 4-HNE to measure lipid peroxidation. Scale bar = 70 μm. (B) Quantification of spinal cord ventral horns stained with 4-HNE as described and shown in A. The 4-HNE fluorescence intensity of untreated and PCA-treated hSOD1G93A littermate mice were normalized and expressed as a percentage of mean 4-HNE fluorescence measured in the WT littermate control mouse. Data are expressed as the mean ± SEM; 6 ventral horns were imaged per mouse. ** indicates p < 0.01 compared to the untreated hSOD1G93A control littermate (paired t-test). Raw mean 4-HNE fluorescence units for the untreated hSOD1G93A mouse (11.70 ± 0.78) × 106) are significantly higher than the WT littermate mouse (7.83 ± 0.16) × 106) (p < 0.01) (D) Quantification of spinal cord ventral horns stained with 4-HNE as described and shown in C. The 4-HNE fluorescence intensity of untreated and PCA-treated hSOD1G93A littermate mice were normalized and expressed as a percentage of mean 4-HNE fluorescence measured in the WT littermate control mouse. Data are expressed as the mean ± SEM; 6 ventral horns were imaged per mouse. * indicates p < 0.05 compared to the untreated hSOD1G93A control littermate (paired t-test). Raw mean 4-HNE fluorescence units for the untreated hSOD1G93A mouse (6.56 ± 0.88) × 106) are significantly higher than the WT (4.17 ± 0.24) × 106) (p < 0.05).