Fig. 9: Cx43 GJ inhibition attenuated RIP1 and MLKL expression in vivo and in vitro via mediating the content of ROS.

a Heptanol (0.1 mg/kg, 1 h before AOLT) attenuated RIP1 and MLKL expression at 8 h after reperfusion. n = 8, *P < 0.05 vs sham; #P < 0.05 vs the AOLT group. Vehicle control of heptanol was DMSO, which had no significant effects on the above-mentioned parameters (data not shown). b Gap26 application (300 μM, 1 h) or NAC application (10 mM, 1 h) attenuated RIP1 and MLKL expression when NRK-52E cells were pretreated with H24R4. n = 8, *P < 0.05 vs control; #P < 0.05 vs the H24R4 group. c Gap26 application (300 μM, 1 h) or NAC application (10 mM, 1 h) attenuated RIP1 and MLKL expression when NRK-52E cells were pretreated with LPS. n = 8, *P < 0.05 vs control; #P < 0.05 vs the LPS group. d Gap26 application (300 μM, 1 h) or NAC application (10 mM, 1 h) attenuated RIP1 and MLKL expression when NRK-52E cells were pretreated with H24R4 + LPS. n = 8, *P < 0.05 vs control; #P < 0.05 vs H24R4 + LPS group