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    Inhibition of Phosphorylated c-Jun NH(2)-terminal Kinase by 2’,4’-dihydroxy-6-methoxy-3,5-dimethylchalcone Isolated from Eugenia aquea Burm f. Leaves in Jurkat T-cells

    Melisa I. Barliana1,2★, Ajeng Diantini3, Anas Subarnas3, Rizky Abdulah2,3, Takashi Izumi4★ Corresponding author

    1. 1Department of Biological Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
    2. 2Center for Drug Discovery and Product Development, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
    3. 3Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor 45363, Indonesia.
    4. 4Department of Biochemistry, Graduate School of Medicine, Gunma University, Gunma Prefecture, Japan.

    CORRESPONDENCE

    Melisa I. Barliana

    Department of Biological Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor 45363, Indonesia.

    melisa.barliana@unpad.ac.id

    Received: 18-01-2017; Revised: 01-03-2017; Accepted: 01-03-2017.

    Volume 13, Issue 51s · pp. S573–7 · PUBLISHED 11 October 2017 · DOI: 10.4103/pm.pm_16_17

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Indonesian medicinal plants have been used for their anticancer activity for decades. However, the therapeutic effects of medicinal plants have not been fully examined scientifically. As cancer is a major health problem worldwide, searching for a new anticancer compound has attracted considerable attention. Our previous study found that 2’,4’‑dihydroxy‑6‑methoxy‑3,5‑dimethylchalcone, an active compound isolated from leaves of Indonesian medicinal plants Eugenia aquea Burm f. (Myrtaceae), had anticancer activity in MCF‑7 human breast cancer cells through induction of apoptosis. Objective: To investigate the molecular mechanism of 2’,4’‑dihydroxy‑6‑methoxy‑3,5‑dimethylchalcone antiproliferative activity. Materials and Methods: Leaves of E. aquea were extracted by ethanol, fractionated by ethyl acetate, n‑hexane, or water, and isolated for its active compound. Jurkat T‑cells were treated with 2’,4’‑dihydroxy‑6‑methoxy‑3,5‑dimethylchalcone for 12 and 24 h, and a cell viability assay and real‑time‑reverse transcriptase polymerase chain reaction for interleukin‑2 (IL‑2) mRNA measurement were performed. The effects of active compound to mitogen‑activated protein kinases were also examined to investigate the mechanism of its antiproliferative activity. Results: 2’,4’‑dihydroxy‑6‑methoxy‑3,5‑dimethylchalcone inhibited Jurkat T‑cell proliferation with a half maximal inhibitory concentration of 59.5 µM. Although IL‑2 mRNA expression was slightly increased after treatment, it inhibited c‑Jun N‑terminal kinase expression but not p38 and extracellular signal‑regulated kinase expression. Conclusions: Our study indicated that the molecular mechanism mediating the antiproliferative activity of 2’,4’‑dihydroxy‑6‑methoxy‑3,5‑dimethylchalcone may be attributed to the stimulation of an immunological microenvironment in the cells.

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      Barliana, M. I., Diantini, A., Subarnas, A., Abdulah, R., & Izumi, T. (2017). Inhibition of Phosphorylated c-Jun NH(2)-terminal Kinase by 2’,4’-dihydroxy-6-methoxy-3,5-dimethylchalcone Isolated from Eugenia aquea Burm f. Leaves in Jurkat T-cells. Pharmacognosy Magazine, 13(51s), S573–7. https://doi.org/10.4103/pm.pm_16_17