Dihydroxy-Isosteviol Methyl Ester from Pulsatilla nigricans Induces Apoptosis in HeLa Cells: Its Cytoxicity and Interaction with Calf Thymus DNA

Dihydroxy‐isosteviol methyl ester (DIME), the principal biological compound isolated from the medicinal plant Pulsatilla nigricans (Fam: Ranunculaceae) having the molecular formula of C21H34O3 (molecular weight 334.25), was administered to cervical cancer cells (HeLa) in vitro to evaluate its possib...

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Bibliographic Details
Published in:Phytotherapy research 2013-05, Vol.27 (5), p.664-671
Main Authors: Das, Sreemanti, Das, Jayeeta, Samadder, Asmita, Khuda-Bukhsh, Anisur Rahman
Format: Article
Language:English
Subjects:
Animals
apoptosis
Apoptosis - drug effects
cancer
Cattle
Cell Survival
circular dichroism spectroscopy
Comet Assay
dihydroxy-isosteviol methyl ester
Diterpenes, Kaurane - chemistry
Diterpenes, Kaurane - pharmacology
DNA - chemistry
DNA Fragmentation - drug effects
HeLa Cells
Humans
Pulsatilla
Pulsatilla - chemistry
Pulsatilla nigricans
Ranunculaceae
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Summary:Dihydroxy‐isosteviol methyl ester (DIME), the principal biological compound isolated from the medicinal plant Pulsatilla nigricans (Fam: Ranunculaceae) having the molecular formula of C21H34O3 (molecular weight 334.25), was administered to cervical cancer cells (HeLa) in vitro to evaluate its possible apoptotic (anti‐cancer) potentials. We analyzed the expression of p53, Bax, Bcl2, Apaf and caspase 3 signal proteins and analyzed the early apoptotic events in HeLa cells induced by DIME using protocols like Annexin V‐FITC and PI staining. DIME caused a significant decrease in cell viability, induced nuclear condensation and inter‐nucleosomal DNA fragmentation. We further studied the interaction of DIME with calf thymus DNA as target through circular‐dichroism spectra. Results showed that DIME interacted with DNA, bringing indiscernible changes in structure and conformation. Thus, DIME showed its capability to induce apoptosis in cancer cells, signifying its utility in drug design as a possible candidate for chemoprevention. Copyright © 2012 John Wiley & Sons, Ltd.
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.4768