A p‐Menth‐1‐ene‐4, 7‐diol (EC‐1) from Eucalyptus camaldulensis Dhnh. Triggers Apoptosis and Cell Cycle Changes in Ehrlich Ascites Carcinoma Cells. (13th January 2015)

• Record Type: Journal Article
• Authors: Islam, Farhadul; Khanam, Jahan Ara; Khatun, Mahbuba; Zuberi, Natasha; Khatun, Laboni; Kabir, Syed Rashel; Reza, Md Abu; Ali, MM; Rabbi, M A; Gopalan, Vinod; Lam, Alfred King‐Yin
• Is Part Of: Phytotherapy research. Volume 29:Number 4(2015:Apr.)
• Page Start: 573
• Page End: 581
• Publication Date: 2015-01-13
• Subjects: Materia medica, Vegetable -- Periodicals; Botany, Medical -- Periodicals; Medicinal plants -- Periodicals; Plant Extracts -- therapeutic use -- Periodicals; Plants, Medicinal -- Periodicals; 581.634
• DOI: 10.1002/ptr.5288
• Languages: English
• ISSNs: 0951-418X

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Anticancer activities of <italic>p</italic>‐menth‐1‐ene‐4, 7‐diol (EC‐1) isolated from <italic>Eucalyptus camaldulensis</italic> Dhnh. were studied on Ehrlich ascites carcinoma (EAC) cells by MTT (3‐[4, 5‐dimethylthiazol‐2‐yl]‐2, 5 diphenyl tetrazolium bromide) assay. Anticancer activities also analyzed in EAC‐bearing mice by assessment of cancer growth inhibition, changes in cancer volume, changes in life span, and hematological parameters. Apoptosis was analyzed by fluorescence microscope, DNA fragmentation assay, and flow cytometry. The expression of apoptosis‐related genes, <italic>Bcl‐2</italic>, <italic>Bcl‐X</italic>, <italic>PARP‐1</italic>, <italic>p53</italic>, and <italic>Bax</italic>, were analyzed using polymerase chain reaction (PCR). EC‐1 significantly inhibited proliferation of EAC cells <italic>in vivo</italic> and restored the altered hematological parameters of EAC‐bearing mice. Cytological observation by fluorescence microscope showed apoptosis of EAC cells upon treatment with EC‐1. Also, DNA fragmentation assay revealed EAC cells' apoptosis following EC‐1 treatment. Increased mRNA expressions of <italic>p53</italic> and <italic>Bax</italic> genes and negative expressions of <italic>Bcl‐2</italic> and <italic>Bcl‐X</italic> were observed in cells treated with EC‐1. These findings confirmed the induction of apoptosis by EC‐1. In addition, MTT assay showed dose‐dependent anticancer activity of EC‐1 against EAC cell. Cell cycle analysis revealed that EC‐1 treatment caused suppression of EAC cells at S phase. To conclude, EC‐1 is a novel anticancer compound and showed antiproliferative and apoptotic activities in cellular and mice models. Copyright © 2015 John Wiley & Sons, Ltd.</p> </abstract>