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ORIGINAL ARTICLE
Year : 2017  |  Volume : 13  |  Issue : 51  |  Page : 573-577

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


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

Correspondence Address:
Melisa I Barliana
Department of Biological Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jl. Raya Bandung-Sumedang Km 21, Jatinangor 45363
Indonesia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_16_17

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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 μ M. 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. Abbreviations used: E. aquea: Eugenia aquea, IL-2: Interleukin-2, MAPK: Mitogen-activated protein kinase, ERKs: Extracellular signal-regulated kinases, JNKs: c-Jun N-terminal kinases, p38: p38 MAPK, PI3K: Phosphatidylinositol-3 kinase, IC50: Half maximal inhibitory concentration.


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