Startseite Medizin Antioxidant and antiproliferative potentials of methanol extract of Xylopia aethiopica (Dunal) A. Rich in PC-3 and LNCaP cells
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Antioxidant and antiproliferative potentials of methanol extract of Xylopia aethiopica (Dunal) A. Rich in PC-3 and LNCaP cells

  • Oluwatosin Adekunle Adaramoye EMAIL logo , Bettina Erguen , Bianca Nitzsche , Michael Höpfner , Klaus Jung und Anja Rabien
Veröffentlicht/Copyright: 24. Mai 2017

Abstract

Background:

Our previous studies showed that fruit methanol extract from Xylopia aethiopica (MEXA) exhibited antiproliferative activity in human cervical cancer cells via the induction of apoptosis. The present study was designed to assess the antiproliferative, antiangiogenic and antioxidant effects of MEXA on prostate cancer (PCa) cells (PC-3 and LNCaP).

Methods:

PC-3 and LNCaP cells were cultured and treated with MEXA (10, 50 and 100 μg/mL). The sodium 3′-[1-(phenylaminocarbonyl)-3,4-tetrazolium]-bis (4-methoxy-6-nitro) benzene sulfonic acid hydrate (XTT) and lactate dehydrogenase (LDH) assays were used to evaluate cell viability and cytotoxicity, respectively. DNA fragmentation was determined by cell death detection ELISA plus, and angiogenesis was assessed by chicken chorioallantoic membrane (CAM) assay. The antioxidant activities of MEXA were determined by DPPH and hydroxyl (OH) radicals’ scavenging methods as well as through the inhibition of lipid peroxidation (LPO) in rats’ liver homogenate.

Results:

MEXA at 100, 250 and 500 μg/mL scavenged DPPH by 48%, 62%, 70% and OH radical by 39%, 58%, 67%, respectively. MEXA significantly (p<0.05) inhibited LPO in a concentration-dependent manner. In addition, MEXA had antiproliferative effects on PC-3 and LNCaP with IC50 of 62.1 and 73.6 μg/mL, respectively, at 96 h. The LDH assay showed that MEXA had low toxicity in vitro at its IC50 values. The extent of DNA fragmentation by MEXA showed higher values in PC-3 and LNCaP, suggesting the possible induction of apoptosis. In contrast, MEXA did not affect the network of vessels in CAM, thus lacking anti-angiogenic property.

Conclusions:

These findings suggest that MEXA induces antiproliferative activity in PCa cells through a mechanism that involves apoptosis. Therefore, MEXA may be a potential therapeutic agent for PCa.


Corresponding author: Dr. Oluwatosin Adekunle Adaramoye, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria, Phone: +234-816-3047-157, Fax: +234-2-810-3043

Acknowledgments

This study was supported by a 6-month grant given to OAA by the Bank-Anthony Charitable Will Trust (London, UK), which was disbursed by the College of Medicine, University of Ibadan, Nigeria and Charite University of Medicine, Berlin, Germany, and by the Urologic Research Foundation Berlin.

  1. Authors’ contributions: Dr. O. A. Adaramoye, Dr. Anja Rabien, and Prof. Michael Höpfner jointly designed the study. Dr. O. A. Adaramoye, Mrs. Bettina Erguen, and Dr. Bianca Nitzsche carried out the studies. Dr. O. A. Adaramoye prepared the manuscript. Prof. Klaus Jung, mentor on this project, corrected and finalized the manuscript. All the authors have accepted responsibility for the entire content of this submitted manuscript and approved its submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organization(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2016-10-19
Accepted: 2017-3-11
Published Online: 2017-5-24
Published in Print: 2017-7-26

©2017 Walter de Gruyter GmbH, Berlin/Boston

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