Key Results
Sinapic acid treatment attenuated the behavioural defects and loss of
dopaminergic neurons in the MPTP mouse model of PD. Sinapic acid also
improved mitochondrial function in MPTP-treated mice, as indicated by
diminished mitochondrial swelling and increased mitochondrial glutamate
dehydrogenase activity. MPTP treatment increased the abundance of
mitochondrial fission proteins such as dynamin-related protein 1 (Drp1)
and phospho-Drp1 Ser616, while sinapic acid treatment attenuated
abnormal mitochondrial fission. In addition, MPTP decreased the
expression of REV-ERB α protein, whereas sinapic acid increased its
expression. To elucidate the molecular mechanism linking REV-ERB α and
mitochondrial fission, we used the pharmacological REV-ERB α inhibitor
SR8278. Sinapic acid and SR8278 co-treatment reversed phospho-Drp1
Ser616 protein expression and the protective effect of sinapic acid in
MPTP-treated mice.