Fig. 3: VNS improved myocardium mitochondrial function and energy production. | Cell Death & Disease

Fig. 3: VNS improved myocardium mitochondrial function and energy production.

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

Fig. 3

A Using gene chip technology, cellular component including mitochondrion, mitochondrial inner membrane, mitochondrial respiratory chain complex I, and mitochondrial proton-transporting ATP synthase complex were markedly improved. Gene chip thermography showed the obvious changes in genes-related mitochondrial function. B and C VNS increased PGC1α expression in infraction area of the infarcted heart as evaluated by PGC1α staining, and mAChR inhibitor Atrop or α7-AChR blocker MLA markedly abolished the effect of VNS on PGC1α expression in infraction area of the infarcted hearts. n = 6, *P < 0.05 vs. Sham; #P < 0.05 vs. MI. @P < 0.05 vs. VNS; &P < 0.05 vs. VNS. D ACh improved mitochondrial mass as evaluated by mean fluorescence intensity (MFI) using MitoTracker® Deep Red FM staining. E ACh improved mitochondrial function as evaluated by ratio of red to green using JC-1staining. F VNS increased the levels of ATP in infarcted heart. n = 6, *P = 0.00001 vs. MI. G ACh increased the levels of ATP in H9C2 cells. n = 6, *P = 0.00012 vs. H/R. For all scatter plots, data are mean ± SEM; one-way ANOVA with Bonferroni post hoc testing.

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