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. Author manuscript; available in PMC: 2020 Sep 18.
Published in final edited form as: ACS Chem Neurosci. 2019 Aug 19;10(9):4018–4030. doi: 10.1021/acschemneuro.9b00271

Figure 8.

Figure 8.

TPPU and EETs prevented Aβ42-induced mitochondrial dysfunction in differentiated SH-SY5Y cells. Cellular mitochondrial membrane potential (Δψm) was evaluated with JC-10 assay. FCCP at 50 μM or Aβ42 at 10 μM depolarized Δψm as indicated by increasing JC-10 monomer/aggregate fluorescence ratio (525/590 nm). Pretreatment with TPPU, EETs, or co-dose for both significantly prevented the depolarized condition of mitochondria in the presence of 10 μM Aβ42 in 72 h. Data were the mean of duplicate of six independent experiments with ± SEM (n = 6). Data were analyzed by one-way ANOVA with Tukey’s multiple comparison test. ####p < 0.0001 relative to the vehicle control; ***p < 0.001, ****p < 0.0001 relative to the 10 μM Aβ42 treatment. FCCP at 50 μM was used as a reference control.