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

Authors

  • 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
Further Information

Publication History

received 12 October 2017
revised 15 March 2018

accepted 19 March 2018

Publication Date:
07 May 2018 (online)

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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.