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. 2018 Feb 20;4:31. doi: 10.1038/s41420-017-0023-4

Fig. 2. TSP-1 prevents Aβ-mediated mitochondrial dysfunction in HT22 cells.

Fig. 2

a HT22 cells were stained with DCFDA dye to measure cellular ROS levels. b TSP-1 completely blocked Aβ-mediated ROS increase. Data were obtained from at least five replicates for each group. Data are presented as mean ± SEM. *p < 0.05 vs. vehicle (DMSO)-treated cells; #p < 0.05 vs. Aβ-treated cells. Scale bar, 50 μm. c MitoSOX reagent was used to detect mitochondrial specific ROS levels. d TSP-1 significantly inhibited Aβ-induced ROS increment. Data were obtained from at least five replicates for each group. Data are presented as mean ± SEM. **p < 0.01 vs. vehicle (DMSO)-treated cells; ##p < 0.01 vs. Aβ-treated cells. Scale bar, 50 μm. ei Seahorse assay using XF analyzer was performed to measure oxygen consumption rate (OCR) after both Aβ only and Aβ + TSP-1 treatment. In addition, basal respiration, ATP production, the maximal capacity of the OXPHOS system, and non-mitochondrial respiration were also measured by calculating the change of the OCR value by oligomycin, FCCP, rotenone, and antimycin A administration, with a seahorse XF analyzer. Data were obtained from at least nine replicates for each group for three independent experiments. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 vs. Aβ-treated cells