Figure 1.

Aβ1-42 induces mitochondrial damage, ROS production, and mitochondrial autophagy in AD-modeled neurons

(A) Expression of mitochondrial-autophagy-related proteins normalized to β-actin in AD-modeled neurons detected by western blot analysis. (B) Binding of autophages to lysosomes in AD neurons by mRFP-GFP-LC3 staining is shown. (C) The mitochondrial membrane potential of AD-modeled neurons by JC-1 staining is shown. (D) Cell ATP production detected in AD neurons is shown. (E) Total ROS production in AD-modeled neurons detected by DCFH-DA staining is shown. DCFH-DA without intrinsic fluorescence can enter into cells through the membrane and then be hydrolyzed into DCFH by esterase. DCFH is incapable of crossing through the cell membrane, such that probes can be easily loaded into cells where active oxygen can oxidize non-fluorescent DCFH to generate DCF with green fluorescence, which indicates the ROS content. (F) ROS production in mitochondria in AD-modeled neurons detected by dihydrorhodamine (DHR) 123 staining is shown. DHR123 was oxidized into rhodamine123 by ROS in the mitochondria, and rhodamine123 was excited at 488 nm while green fluorescence was emitted at 515 nm. Measurement data were expressed in the form of mean ± standard deviation. The comparison between two groups was performed by independent sample t test. ∗p < 0.05. The experiment was repeated three times independently.