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.