Fig. 8
Propofol inhibited the activation of RhoA/LIMK2/cofilin and RhoA/MLCK signaling pathways. A Levels of P-LIMK2, LIMK2, P-cofilin and cofilin on HUASMCs were tested by western blot. GAPDH served as a loading control. n = 4 per group. B Levels of MLCK on HUASMCs were tested by western blot. GAPDH served as a loading control. n = 3 per group. C Levels of p-LIMK2, LIMK2, p-cofilin and cofilin on HUASMCs were tested by western blot. GAPDH served as a loading control. n = 3 per group. D Levels of MLCK on HUASMCs were tested by western blot. GAPDH served as a loading control. n = 3 per group. *p < 0.05, ** p < 0.01, *** p < 0.001. All values expressed as mean ± SEM. E The scheme of the mechanism that propofol induces excessive relaxation in Ang II-HUASMCs. (1) Comparison of the number and function of Cx43-GJs and [Ca2+]i in normal and Ang II-HUASMCs. (2) ①When HUASMCs are treated with propofol, propofol causes a prominent decrease in the function of Cx43-GJs in Ang II-HUASMCs compared with normal HUASMCs; ② This results in a more substantial decrease of intracellular Ca2+ mobility in Ang II-HUASMCs; ③-④ Subsequently, propofol also leads to a stronger inhibition on the activation of RhoA protein and its downstream- RhoA/LIMK2/cofilin and RhoA/MLCK signaling pathways in Ang II-HUASMCs; ⑤ Ultimately, compared to normal HUASMCs, the activation of F-actin polymerization and MLC2 phosphorylation were both mitigated more dramatically in Ang II-HUASMCs, which caused excessive relaxation