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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: HSF1 is involved in suppressing A1 phenotype conversion of astrocytes following spinal cord injury in rats

Fig. 7

Western blot analysis of HSF1 agonist 17-AAG on the activation of ERK (a, b), P38 (a, c), JNK (a, d), and NFκB (a, e) following cell incubation at ACM for 24 h in the presence of 0.5 μmol/L 17-AAG. Quantities were normalized to endogenous β-actin. Experiments were performed in triplicates. Error bars represent the standard deviation, *P < 0.05, #P < 0.05, one-way ANOVA with Tukey’s post hoc test. For quantitative analysis of ERK activation, F (4, 10) = 39.91, P < 0.001. ACM vs con, P = 0.0003; 17-AAG + DMSO vs ACM, P < 0.0001; 17-AAG + ACM + DMSO vs ACM, P < 0.0001. For quantitative analysis of P38 activation, F (4, 10) = 14.52, P = 0.0004. ACM vs con, P = 0.0056; 17-AAG + DMSO vs ACM, P = 0.0053; 17-AAG + ACM + DMSO vs ACM, P = 0.0059. For quantitative analysis of JNK activation, F (4, 10) = 16.46, P = 0.0002. ACM vs con, P = 0.0097; 17-AAG + DMSO vs ACM, P = 0.0006; 17-AAG + ACM + DMSO vs ACM, P = 0.0112. For quantitative analysis of NFκB activation, F (4, 10) = 76.38, P < 0.0001. ACM vs con, P < 0.0001; 17-AAG + DMSO vs ACM, P < 0.0001; 17-AAG + ACM + DMSO vs ACM, P < 0.0001

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