Nicotinamide riboside chloride (NRC) treatment ameliorated mitochondrial dysfunction and mitochondrial oxidative stress. (IMAGE)
Caption
(A) ATP content of the mouse hippocampus. (B) Mitochondrial complex IV activity of the mouse hippocampus. (C, D) Transmission electron microscopy analysis of mitochondrial alterations in mouse brain tissue following alcohol exposure and NRC supplementation. (E, F) Significant improvement in mitochondrial permeability transition pore (MPTP) was observed after NRC treatment. (G, I) Mitochondrial membrane potential. (H, J) Mitochondrial ROS production. (K) ATP content of HT22 cells. (L) Mitochondrial complex IV activity of HT22 cells. (M, N) Mitochondrial integrity was used to detect changes in mitochondrial dynamics in the negative control (NC) group, NRC group, alcohol group, and the alcohol plus NRC group, and the average length of mitochondria in cells was measured (scale bar: 50 μm). The results were shown by the representative images and their corresponding quantitative results. Each group included three mice, with three independent replicates performed. Each value was expressed as mean ± standard deviation (n = 3 independent experiments). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.
Credit
Jinyang Wang, Jianan Wang, Wei Xie, Qi Shen, Chengbin Wang, Ruibing Li, Shixiong Deng
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