Fig. 4: VNS improved cardiomyocytes metabolic process in infracted heart through m/n-AChR. | Cell Death & Disease

Fig. 4: VNS improved cardiomyocytes metabolic process in infracted heart through m/n-AChR.

From: Vagus nerve stimulation optimized cardiomyocyte phenotype, sarcomere organization and energy metabolism in infarcted heart through FoxO3A-VEGF signaling

Fig. 4

A and B Typical image of CPT1α and GLUT4 in VNS-MI hearts with or without the treatment of mAChR inhibitor atropine (Atrop) or α7-AChR blocker mecamylamine (MLA) as determined by immunohistochemically staining. C–F VNS increased CPT1α and GLUT4 in infraction area of the infarcted heart as evaluated by western blot, and mAChR inhibitor Atrop or α7-AChR blocker MLA markedly abolished the effect of VNS on CPT1α and GLUT4 expressions in infraction area of the infarcted hearts. n = 3, *P < 0.05 vs. Sham; #P < 0.05 vs. MI; @P < 0.05 vs. VNS. &P < 0.05 vs. VNS. For all scatter plots, data are mean ± SEM; one-way ANOVA with Bonferroni post hoc testing.

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