Fig. 7
From: Neuroprotective effect of Apelin 13 on ischemic stroke by activating AMPK/GSK-3β/Nrf2 signaling
The activation effects of Apelin 13 on AMPK is through AR/Gα/PLC/IP3/CaMKK. PC12 cells were pretreated with Apelin 13 with or without Gαq inhibitor Gp2A (10 μM) and Gαi inhibitor pertussis toxin (PTX) (200 ng/ml), then exposed to the indicated conditions. Cell viability (a) and ROS levels (b) were measured using relative kit. c Gp2A and PTX abolished the effects of Apelin 13 on the activation of AMPK/GSK-3β/Nrf2 pathway. d Apelin 13 induced the expression of PLC, IP3, and CaMKK in a dose-dependent manner. e PC12 cells were pretreated with Apelin 13 with or without CaMKK inhibitor STO-609 (1 μg/ml) and IP3 inhibitor 2-APB (1 μg/ml), then exposed to the indicated conditions. The phosphorylation of AMPK and GSK-3β (e) and the expression of CaMKK (f) were determined by western blotting. g PC12 cells were pretreated with Apelin 13 with or without apelin receptor inhibitor F13A (1 μM), then exposed to the indicated conditions. F13A inhibited the expression of PLC, IP3, CaMKK (g) and the phosphorylation of AMPK and GSK-3β (h) and increased the ROS levels (i) in PC12 cells. The columns and error bars were represented as means ± SD. ##P < 0.01 vs. the control group; **P < 0.01 vs. the I/R treatment group. &&P < 0.05 vs. the Apelin 13 treatment group