Fig. 6: Efficacy of C-Mn3O4 NPs in the protection of mitochondria, the master redox regulator in mice.
From: Redox nanomedicine ameliorates chronic kidney disease (CKD) by mitochondrial reconditioning in mice
a Ca2+ induced mPTP opening measured by the decrease in 540 nm absorbance. b Mitochondrial membrane potential (Δψm) estimated using JC-1 fluorescence. c ATP content. d Cytochrome c oxidase (complex IV in the electron transport chain, ETC) activity in isolated mitochondria. e Succinate dehydrogenase (SDH, complex II in ETC) activity in isolated mitochondria. f DNA fragmentation level as a result of oxidative damage measured using agarose gel electrophoresis. In cisplatin-induced CKD animals DNA ladder formation, indicative of apoptotic DNA fragmentation, is clearly visible. The corresponding stacked bar plot shows the relative abundance of different-sized fragmented DNA in relation to the total DNA content of the lane. g Schematic overview of the comprehensive molecular mechanism of action of C-Mn3O4 NPs as a redox medicine against cisplatin-induced CKD. The numbers in the black circles indicate the sequence of events. In bar plots data were expressed as Mean ± SD. Violins depict kernel density estimation of the underlying data distribution with the width of each violin scaled by the number of observations at that Y-value. Three lines (from the bottom to the top) in each violin plot show the location of the lower quartile (25th), the median, and the upper quartile (75th), respectively. The shaded area indicates the probability distribution of the variable. Individual data points are represented as colored circles (N = 10). One-way analysis of variance (ANOVA) followed by Tukey’s post hoc multiple comparison test was performed for comparison among the groups. The numbers inside the plots indicate numerical p values. p < 0.05 is considered significant.
