Planta Med 2018; 84(14): 1007-1012
DOI: 10.1055/a-0595-7899
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Ombuoside from Gynostemma pentaphyllum Protects PC12 Cells from L-DOPA-Induced Neurotoxicity

Uchralsaikhan Davaasambuu*
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
,
Hyun Jin Park*
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
2  Research Center for Bioresource and Health, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
,
Keun Hong Park
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
,
Chong Kil Lee
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
2  Research Center for Bioresource and Health, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
,
Bang Yeon Hwang
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
,
Myung Koo Lee
1  Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
2  Research Center for Bioresource and Health, College of Pharmacy, Chungbuk National University, Cheongju, Republic of Korea
› Author Affiliations
Further Information

Publication History

received 12 October 2017
revised 15 March 2018

accepted 19 March 2018

Publication Date:
07 May 2018 (online)

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.

* These authors contributed equally to the study.