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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Therapeutic blockade of HMGB1 reduces early motor deficits, but not survival in the SOD1G93A mouse model of amyotrophic lateral sclerosis

Fig. 1

Pre-onset anti-HMGB1 2G7 treatment improves early hind-limb grip strength deficit, but does not extend survival in SOD1G93A transgenic mice. SOD1G93A mice were intraperitoneally injected weekly with the anti-HMGB1 antibody at 35 days of age (red line). a Left panel shows a Kaplan-Meier plot of ages (in days) in which SOD1G93A mice treated with isotype control (vehicle, 100 μg; orange line) or anti-HMGB1 antibody (100 μg; blue line) reached end-stage of disease (complete hind-limb paralysis and an inability to right itself once placed on its back; n = 13, P = 0.362, log-rank test). Anti-HMGB1 treatment at 35 days of age (100 μg) resulted in no extension in survival time compared with vehicle treatment. a Right panel shows the end-stage survival age for each litter-matched pair of vehicle- and anti-HMGB1-treated SOD1G93A mice. b, c Shows no differences in body weight and motor score between vehicle (orange line) and anti-HMGB1 (blue line) treated SOD1G93A mice (n = 13, P > 0.05, two-way ANOVA). d Shows an early transient improvement in hind-limb grip strength for anti-HMGB1-treated versus vehicle-treated SOD1G93A mice at 56 and 63 days of age (n = 13, *p < 0.05, +p < 0.0001, two-way ANOVA with post-hoc Bonferroni’s multiple comparisons test). Data are expressed as mean ± SEM

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