Fig. 3.

Activation of ER stress and the MAPK-mediated inflammatory pathway in the perithalamic lesion site of CPSP rats. a, b Representative Western blot bands and quantification of ER stress markers in the perilesion site of sham and CPSP group were presented. The abundance of ER stress markers, including BIP, p-IRE1α, p-PERK, and ATF6 and their downstream targets p-eIF2α and sXbp1, are significantly elevated along the thalamic lesion site during the 1-month observation period after CPSP compared with the sham control. Values are expressed as mean ± SD. The expression of ER stress markers in the sham group were set as 1 for quantification purpose. A scatter plot with a bar chart displays the target expression normalized to Tublin. The levels of phosphorylation are normalized to the total protein. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n = 5 rats per group, one-way ANOVA followed by Bonferroni post hoc test. c Electron microscopic observation of the subcellular morphological change of the neurons around the lesion site on day 14 after CPSP induction. The white rows indicate the normal ER, whereas the red arrows show the swollen ER after lesion. Scale bars = 1 μm. d, e Representative Western blot bands and quantification of JNK and p38 in the perilesion site of sham and CPSP group were presented. The expression of JNK and p38 in the sham group were set as 1 for quantification purposes. A scatter plot with a bar chart displays the target expression normalized to Tublin. The levels of phosphorylation are normalized to the total protein. Phosphorylation of JNK and p38 are significantly increased along the thalamic lesion site, indicating that the MAPK-associated inflammatory pathway is activated after CPSP. Values are expressed as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ***P < 0.0001, compared with sham control, n = 5 per group, one-way ANOVA with the Bonferroni post hoc test