Fig. 7

SR-A1 is essential for AMPK-mediated reduction of HMGB1 accumulation and MMP-9 activity. A–C The expression of SR-A1, p-AMPK or p-PKC in DRG of mice treated with metformin (200 mg/kg, i.p.) at present of AMPK inhibitor (CC, 25 mg/kg, i.p.) or PKC inhibitor (Go6983, 4 mg/kg, i.p.) (n = 3). Mechanical thresholds of mice treated with metformin (200 mg/kg, i.p.) in the presence of CC (D), Go6983 (E) or SR-A1 KO (F) (n = 8). HMGB1 content and MMP-9 activity in plasma of mice treated with metformin (200 mg/kg, i.p.) in the presence of CC (G, J) (n = 5), Go6983 (H, K) (n = 5) or SR-A1 KO (I, L) (n = 3). Mice or SR-A1 KO mice were administrated with L-OHP injection (3 mg/kg, i.p., five consecutive days). Metformin (200 mg/kg, i.p. q.d) or vehicle was injected for 14 days, starting from a day before the first injection of L-OHP. CC and Go6983 were administered once daily for 5 days, 30 min before the administration of metformin. Plasma (G–I) and DRG (A–C) were collected after the final treatment of metformin for western blotting (A–C, G–I) or gelatin zymography (J–L). Representative bands and a data summary (n = 4 for each group) are shown. Significant differences were revealed following one-way or two-way ANOVA (*p < 0.05, **p < 0.01 and ***p < 0.001 vs. Control; ^#p < 0.05, ^##p < 0.01 and ^###p < 0.001 vs. L-OHP group; ^&p < 0.05, ^&&p < 0.01 and ^&&&p < 0.001 vs. L-OHP + metformin group; Bonferroni post hoc tests)