Fig. 5.

Reduction of cPLA₂α upregulation in the spinal cord of hmSOD1 mice shortly before the onset of motor dysfunction reduced neuronal death and gliosis. Fifteen-week-old hmSOD1 mice were brain infused with 10 μg/day AS or the corresponding sense for 3–4 weeks and analyzed at week 18–19. a Representative immunofluorescence staining of cPLA₂α, neurons (NeuN), microglia (Iba-1), and astrocytes (GFAP) in the spinal cord tissue section of WT mice, hmSOD1 mice (ALS), hmSOD1 mice brain infused with AS (ALS + AS) or sense (ALS + SE) at 18–19 weeks. Scale bars = 50 μm. Shown are representative images of 12 mice in each group. The mean ± SEM of the fluorescence intensity (for cPLA₂α) and percentage of the cell area (for cell markers) are presented in the bar graph. *p < 0.001—significance from WT mice and from AS-treated hmSOD1 mice. b Representative immunoblot analysis of cPLA₂α, COX-2, and iNOS and the corresponding calreticulin protein expression in the spinal cord lysates of the mice. Densitometry analysis for the three proteins was done as described for cPLA₂α in Fig. 3b. The bar graph is the mean ± SE of 8 mice in each group. *p < 0.001—significance from WT mice and from AS-treated hmSOD1 mice