Celastrus paniculatus seed extract exhibits neuroprotective effects against MPP+‑induced apoptotic cell death via GSK‑3β in a Parkinson's disease model.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease induced by the death of dopaminergic neurons. Seed oil of Celastrus paniculatus (CP) Willd. has protective and antioxidant properties; however, to the best of our knowledge, no studies have analyzed the neuroprotective effect of CP seeds on PD. The present study aimed to investigate the neuroprotective effects and mechanism of CP seed extract (CPSE) using an in vitro 1-methyl-4-phenylpyridinium ion (MPP+)-induced PD model. The effect of CPSE on the expression levels of apoptotic marker proteins, such as Bcl-2 and its upstream pathway protein, glycogen synthase kinase-3β (GSK-3β), was investigated in human neuroblastoma SH-SY5Y cells. The effect of CPSE on the viability of SH-SY5Y cells was evaluated using MTT assay. To investigate the potential neuroprotective effect of CPSE, SH-SY5Y cells were treated with MPP+ to induce PD-associated cytotoxicity. SH-SY5Y cells were treated with 2 mM MPP+ before or after CPSE treatment to determine the protective effect of CPSE against MPP+-induced neurotoxicity using MTT, WST-1 and lactate dehydrogenase assays. Moreover, it was investigated whether CPSE could promote survival signals by regulating the protein expression levels of apoptotic markers (Bcl-2 and GSK-3β) using western blotting. High concentrations and prolonged treatment of CPSE did not have any adverse effect on SH-SY5Y cell viability. Furthermore, MPP+-induced dopaminergic neuron damage was ameliorated by CPSE treatment. CPSE also showed anti-apoptotic activity by reversing the inhibitory effects of MPP+ on Bcl-2 expression. Moreover, CPSE abolished MPP+-induced decreases in phosphorylated-GSK-3β (Ser9) expression. Taken together, the present findings suggested that CPSE may exert a neuroprotective effect in PD.