Abstract
This study investigated the effects of ombuoside on L-3,4-dihydroxyphenylalanine (L-DOPA)-induced
neurotoxicity in PC12 cells. Ombuoside did not affect cell viability at concentrations
of up to 50 µM for 24 h, and ombuoside (1, 5, and 10 µM) significantly inhibited L-DOPA-induced
(100 and 200 µM) decreases in cell viability. L-DOPA (100 and 200 µM) induced sustained
phosphorylation of extracellular signal-regulated kinases (ERK1/2) for 6 h, which
were significantly decreased by cotreatments with ombuoside (1, 5, and 10 µM). L-DOPA
(100 and 200 µM) alone significantly increased c-Jun N-terminal kinase (JNK1/2) phosphorylation
for 6 h and cleaved-caspase-3 expression for 24 h, both of which were partially, but
significantly, blocked by ombuoside (1, 5, and 10 µM). In addition, ombuoside (1,
5, and 10 µM) significantly restored the L-DOPA-induced (100 and 200 µM) decrease
in superoxide dismutase (SOD) activity for 24 h. Taken together, these findings indicate
that ombuoside protects against L-DOPA-induced neurotoxicity by inhibiting L-DOPA-induced
increases in sustained ERK1/2 and JNK1/2 phosphorylation and caspase-3 expression
and L-DOPA-induced decrease in SOD activity in PC12 cells. Thus, ombuoside might represent
a novel neuroprotective agent that warrants further study.
Key words
Ombuoside -
Gynostemma pentaphyllum
- Cucurbitaceae - L-DOPA-induced neurotoxicity - sustained ERK1/2 phosphorylation
- PC12 cells
