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Fig. 6 | Journal of Neuroinflammation

Fig. 6

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

Fig. 6

Immune and inflammatory markers are not altered in tibialis anterior and gastrocnemius muscle of anti-HMGB1 antibody-treated SOD1G93A mice. SOD1G93A mice were intraperitoneally injected weekly with the anti-HMGB1 antibody at 35 days of age (100 μg). Pro-inflammatory cytokines (TNFα and IL-1β) and major innate immune receptors (RAGE, C5aR1 and TLR4) in tibialis anterior (TA) and gastrocnemius (GN) muscle of vehicle and anti-HMGB1-treated SOD1G93A mice was investigated at mid-symptomatic stage of disease (133 days) using quantitative PCR. a, b Shows no change in pro-inflammatory cytokines Tnf and Il1β in both TA and GN muscle of anti-HMGB1-treated SOD1G93A mice when compared to isotype control-treated SOD1G93A mice (n = 6, p > 0.05, Student’s t test). Ager and C5ar1 mRNA transcript levels were not different in isotype control and anti-HMGB1-treated SOD1G93A mice in both TA and GN muscle (c, d; n = 6, p > 0.05, Student’s t test). While anti-HMGB1 treatment showed a slight reduction in Tlr4 transcript levels in TA muscle, no change was observed in GN muscle of SOD1G93A mice (e; n = 6 *p < 0.05, Student’s t test). Data are presented as mean ± SEM

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