Research Paper Volume 13, Issue 8 pp 12160—12178

Balasubramide derivative 3C attenuates atherosclerosis in apolipoprotein E-deficient mice: role of AMPK-STAT1-STING signaling pathway

3C induces AMPK phosphorylation and inhibits JAK2-STAT1 signaling. (A) 3C dose-dependently induced AMPK phosphorylation. (B) 3C time-dependently induced AMPK phosphorylation. (C) 3C time-dependently inhibit IFN-γ induced JAK2 and Stat1 phosphorylation. (D) 3C dose-dependently inhibit IFN-γ induced JAK2 and Stat1 phosphorylation. Cells were pre-treated at indicated different time or with different concentrations of P2 for 4h followed by 10ng/mL IFN-γ incubation for 30min then the cell was harvested. (E) 3C activate AMPK and inhibit IFN-γ stimulated JAK2-Stat1 signaling but IFN-γ has no effect on AMPK. (F) Relative level of P-AMPK, P-JAK2 and P-Stat1 normalized to β-Actin (n=3 per group). All experiments were performed at least three times; were assessed using Student’s t-test and are present as mean±SEM. *P**P

Figure 5. 3C induces AMPK phosphorylation and inhibits JAK2-STAT1 signaling. (A) 3C dose-dependently induced AMPK phosphorylation. (B) 3C time-dependently induced AMPK phosphorylation. (C) 3C time-dependently inhibit IFN-γ induced JAK2 and Stat1 phosphorylation. (D) 3C dose-dependently inhibit IFN-γ induced JAK2 and Stat1 phosphorylation. Cells were pre-treated at indicated different time or with different concentrations of P2 for 4h followed by 10ng/mL IFN-γ incubation for 30min then the cell was harvested. (E) 3C activate AMPK and inhibit IFN-γ stimulated JAK2-Stat1 signaling but IFN-γ has no effect on AMPK. (F) Relative level of P-AMPK, P-JAK2 and P-Stat1 normalized to β-Actin (n=3 per group). All experiments were performed at least three times; were assessed using Student’s t-test and are present as mean±SEM. *P<0.05; **P<0.01.