Evaluation of the Antioxidant Activity and Antiproliferative Effect of the Jaboticaba (Myrciaria cauliflora) Seed Extracts in Oral Carcinoma Cells

doi:10.1155/2014/185946

CNU IR > Pharmacy and Science > Dept. of Cosmetic Science and institute of cosmetic science > Periodical Articles > Item 310902800/28571

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/28571

Title:	Evaluation of the Antioxidant Activity and Antiproliferative Effect of the Jaboticaba (Myrciaria cauliflora) Seed Extracts in Oral Carcinoma Cells
Authors:	Wang, Wen-Hung Tyan, Yu-Chang Chen, Zong-Shiow Lin, Ching-Gong Yang, Ming-Hui Yuan, Shyng-Shiou Tsai, Wan-Chi
Contributors:	化粧品應用與管理系
Keywords:	APOPTOSIS SURVIVIN CANCER FRUITS ACID ANTHOCYANINS PROTEINS CLEAVAGE RELEASE PATHWAY
Date:	2014
Issue Date:	2015-05-06 21:21:06 (UTC+8)
Publisher:	Hindawi Publishing Corporation
Abstract:	It is becoming increasingly evident that certain phytochemicals possess cancer chemopreventive properties. In this study, the antiproliferative activity of extracts from different parts of the jaboticaba (Myrciaria cauliflora) plant was evaluated for its effect on human oral carcinoma cell lines. The cytotoxicities of various plant extract concentrations were examined and the 50% maximal inhibitory concentration (IC50) was determined. Water extracts of jaboticaba seeds showed concentration-dependent antiproliferative effects. Annexin V/propidium iodide positivity with active caspase-3 induction indicated that the treated cells underwent apoptosis. Several important regulatory proteins (Bcl-2, Bcl-xL, Bid, and survivin) involved in apoptosis were also evaluated. The antioxidant activity of jaboticaba was investigated using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azinobis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) assays, and the drug concentration eliciting 50% maximum stimulation (SC50) was determined. The present findings suggest that water extracts of jaboticaba seeds exhibit an antiproliferative effect against oral cancer cells by inducing apoptosis through downregulating survivin expression and thereby activating caspase-mediated Bid cleavage.
Relation:	Biomed Research International, 185946
Appears in Collections:	[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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