Inhibition of α-Synuclein Accumulation Improves Neuronal Apoptosis and Delayed Postoperative Cognitive Recovery in Aged Mice

Figure 7

α-syn inhibition protected mitochondria against lipopolysaccharide-induced dysfunction in neuronal cells. α-syn inhibition in both cell models was performed with transfected Lv-shSnca for 48 h following lipopolysaccharide (LPS) exposure. (a and b) Transmission electron microscopy was used to examine mitochondrial morphology in nerve growth factor- (NGF-) differentiated PC12 cells (a) rat primary hippocampal neurons (b). . (c) Mitochondrial membrane potential (ΔΨm) was assessed using JC-1 (10 μg/mL) in both neuronal cells. . (d) Fluorescent intensity was analyzed. (e) Total cellular reactive oxygen species production detected with DCFH-DA in NGF-differentiated PC12 cells (upper) and rat primary hippocampal neurons (lower); . ATP generation was assessed in NGF-differentiated PC12 cells (f) and rat primary hippocampal neurons (g) using a luminometric assay. Data are expressed as (one-way analysis of variance, ). , , control (Con) vs. LPS or LPS+Lv-shControl; ^#, ^##, LPS+Lv-shControl vs. LPS+Lv-shSnca.

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