Effect of SA on the protein expression of mitochondrial fission
in C57BL/6 mice with MPTP-induced neurotoxicity
Mitochondria easily maintain their homeostasis through several
maintenance mechanisms, such as mitochondrial fission. However,
excessive and aberrant mitochondrial fission promotes mitochondrial
fragmentation and dysfunction, which are associated with the pathology
of a number of neurodegenerative diseases (Qi, Qvit, Su & Mochly-Rosen,
2013). In this study, MPTP treatment tended to increase Drp1 protein
expression, while SA treatment reversed this increase (Figure 4A).
Interestingly, the activated form of Drp1, phospho-Drp1 Ser617,
significantly increased 1.9-fold in MPTP-treated mice compared with that
in the control group, but the inactivated form of Drp1, phospho-Drp1
Ser637, did not change (Figure 4B and C). This increase was attenuated
by SA. Furthermore, the ratio of phospho-Drp1 Ser616/637 also increased
in the MPTP group, while the 40 µM SA treatment group showed
normalization of this ratio (Figure 4D).