Endang Purwaningsih
Department of Anatomy, Faculty of Medicine, YARSI University

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Journal : Universa Medicina

Cytotoxicity assay of Typhonium flagelliforme Lodd against breast and cervical cancer cells Endang Purwaningsih; Etty Widayanti; Yulia Suciati
Universa Medicina Vol. 33 No. 2 (2014)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2014.v33.75-82

Abstract

BACKGROUNDCancer is one of the causes of high mortality. Breast and cervical cancers are two of the most frequent cancers affecting women around the world, including Indonesia. Natural materials such as rodent tuber (Typhonium flagelliforme) have anticancer potentials. The rodent tuber extract contains ribosome inactivating proteins (RIPs) capable of cutting the DNA or RNA of cancer cells and blocking the growth of cancer cells. The purpose of this study was to evaluate the cytotoxic effects of Typhonium flagelliforme Lodd extract on HeLa cervical cancer and Michigan Cancer Foundation-7 (MCF-7) breast cancer cells.METHODSSubjects were cultured cell lines of HeLa cells in Rosswell Park Memorial Institute (RPMI) and of MCF-7 cells in Dulbecco’s Minimum Essential Medium (DMEM). Rodent tuber ethanolic extract was diluted in dimethyl sulfoxide (DMSO). The cytotoxicity assay used the 3-(4,5-dimethyl thiazol-2-yl,5-diphenyl) tetrazolium bromide (MTT) method. Absorbance was read in an ELISA reader at a wavelength of 595 nm.RESULTSRat tuber extract at all dilutions (500; 250; 125; 62.5; 31.25; 15.625;7.81; 3.9 ì g/ mL) showed cytotoxic effects against HeLa and MCF-7 cells. Higherconcentrations of the extract gave a higher proliferation inhibition effect.Calculated IC50 values of the extract by probit analysis were 30.19 ìg/mL against HeLa cells and 5.586 ì g/mL against MCF-7 cells.CONCLUSIONSEthanolic extract of Typhonium flagelliforme Lodd has cytotoxic effects against HeLa cells and MCF-7 cells. The cytotoxic effects against MCF-7 cells are greater than the cytotoxic effects against HeLa cells.
Curcumin inhibits luteal cell steroidogenesis by suppression of extracellular signal regulated kinase Endang Purwaningsih; Sri Kadarsih Soejono; Djaswadi Dasuki; Edy Meiyanto
Universa Medicina Vol. 31 No. 2 (2012)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2012.v31.73-80

Abstract

BackgroundCurcumin inhibits steroidogenesis in luteal cell cultures by inhibiting progesterone secretion. The site of action of curcumin on steroidogenesis in luteal cell cultures is as yet unkown. The purpose of this study was to determine the influence of curcumin on phosphorylation of extracellular signal regulated kinase (ERK) in steroidogenesis of luteal cell cultures.     Methods An experimental study with control was conducted to investigate the site of action of curcumin by measurement of ERK phosphorylation in luteal cell cultures (LCC) after administration of luteinizing hormone (LH) and/or prostaglandin F2 alpha (PGF2á). The subjects of this study were luteal cell cultures derived from the corpus luteum of Sprague Dawley rat with superovulation induced by pregnant mare serum gonadotropin. The luteal cell cultures were devided into 16 groups, both with and without the addition of forskolin and each group contained 4 replicates samples. Curcumin was administered immediately following LH and/or PGF2á stimulation with or without addition of forskolin. The cell culture was then incubated for 24 h. ERK phosphorylation was measured by immunohistochemistry. Data on ERK phosphorylation was analyzed using one-way Anova, followed by multiple comparison tests.     ResultsLH significantly increased ERK phosphorylation, whereas PGF2á significantly reduced ERK phosphorylation. Forskolin significantly increased ERK phosphorylation to a similar degree as LH. Curcumin inhibited ERK phosphorylation in both LH and forskolin-stimulated luteal cell cultures. ConclusionCurcumin inhibits ERK phosphorylation in luteal cell cultures by suppressing signal transduction upstream of ERK.