Fig. 7: NAD+ supplementation attenuates Hcy-induced cognitive inpairment and mitochondrial dysfunction in rats. | Cell Death & Disease

Fig. 7: NAD+ supplementation attenuates Hcy-induced cognitive inpairment and mitochondrial dysfunction in rats.

From: Homocysteine interferes with Ndufa1 leading to mitochondrial dysfunction through repression of the NAD+/Sirt1 pathway in the brain: a possible link between hyperhomocysteinemia and neurodegeneration

Fig. 7

A The 24 2-month-old male SD rats were randomly divided into 3 groups as Con, Hcy, and Hcy+NAD+. B–F MWM showed that Hcy+NAD+ rats had better spatial memory and learning ability than HHcy rats. G, H Typical dendrites of tertiary branch hippocampal pyramidal neurons with Golgi staining and quantitative examination of the overall density of dendritic spines and the density of thin-shaped and mushroom-shaped spines in the hippocampus CA1 region (n = 5 for each group, 2 neurons per rat). I, J Expression of GluN2A, GluN2B, GluN1, PSD95, and SYN1 was measured by western blotting (n = 6 for each group). K, L Cleaved Caspase3 was used to stain the CA1 region of the hippocampus and cortex in rats (n = 6 for each group). M, N Expression of COX5A, SDHB, UQCRC2, and ATP5A in the hippocampus of Con, Hcy, and Hcy+NAD+ rats was measured by western blotting (n = 6 for each group). O, P The relative ATP and ROS levels in the hippocampus were measured using the corresponding kits (n = 6 for each group). Data were presented as mean ± SEM. Two-way repeated measures ANOVA followed by Bonferroni’s post hoc test for (B). One-way ANOVA followed by Bonferroni’s post hoc was used for others (*P < 0.05, **P < 0.01, ***P < 0.001, ns no significance; n = 8 for each group).

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