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. 2023 Jul 3;26(7):107268. doi: 10.1016/j.isci.2023.107268

Figure 3.

Figure 3

QHRD106 protected against stroke via B2R by decreasing HMGB1 translocation and secretion

(A–C) The brains of mice in the saline group and QHRD106 group 3 days after MCAO were analyzed in a proteomics experiment. (A) Heatmap of DEPs between the saline group and the QHRD106 group. (B) KEGG pathway analysis of DEPs. (C) GO analysis of the DEPs, including three categories: biological processes, cellular components, and molecular functions.

(D–F) The nucleocytoplasmic translocation of HMGB1 was evaluated by western blot analysis. GAPDH and Lamin B1 were used as cytoplasmic and nuclear loading controls, respectively.

(G) Serum HMGB1 levels were evaluated by ELISA in mice 7 days poststroke.

All data are presented as the mean ± SEM. Statistical analyses were performed by one-way ANOVA followed by Tukey’s post hoc test. ∗p < 0.05, ∗∗p < 0.01 vs. the saline group; #p < 0.05, ##p < 0.01 vs. the QHRD106 group, “ns” indicates no significance (p > 0.05).