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Licensed Unlicensed Requires Authentication Published by De Gruyter February 1, 2018

Chromatographic fingerprint analysis, antioxidant properties, and inhibition of cholinergic enzymes (acetylcholinesterase and butyrylcholinesterase) of phenolic extracts from Irvingia gabonensis (Aubry-Lecomte ex O’Rorke) Baill bark

  • Oluwafemi Adeleke Ojo EMAIL logo , Adebola Busola Ojo , Basiru Olaitan Ajiboye , Babatunji Emmanuel Oyinloye , Ayodele Jacob Akinyemi , Mary Abiola Okesola , Aline Augusti Boligon and Marli Matiko Anraku de Campos

Abstract

Background:

Irvingia gabonensis stem bark is a medicinal plant used in most parts of Africa to manage a number of ailments including neurodegenerative diseases that occur without scientific basis. This work characterized the phenolic composition, evaluated the cholinergic enzymes (acetylcholinesterase, AChE and butyrylcholinesterase, BChE) inhibition, and assessed the antioxidant activity of phenolic extracts from I. gabonensis (Aubry-Lecomte ex O‘Rorke) Baill bark.

Methods:

Total phenol and flavonoids content was evaluated in addition to antioxidant activity as shown by Fe2+ chelation, 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging ability, and 2,2-azino-bis-(3-ethylbenthiazoline-6-sulfonic acid) (ABTS) radical scavenging ability. Inhibitory activities on AChE and BChE were evaluated.

Results:

The extract was found to be rich in phenolic acid (ellagic acid) and flavonoids (quercetrin, kaempferol, and apigenin). The phenolic extracts displayed DPPH radical scavenging ability (IC50=19.98 μg/mL), ABTS radical scavenging ability (IC50=18.25 μg/mL), iron chelation (IC50=113.10 μg/mL), and reducing power (Fe3+ to Fe2+) (5.94 mg ascorbic acid equivalent/100 g). Extracts of I. gabonensis inhibited AChE (IC50=32.90 μg/mL) and BChE (IC50=41.50 μg/mL) activities in concentration-dependent manner.

Conclusions:

Hence, possible mechanism through which the stem bark executes their anti-Alzheimer’s disease activity might be by inhibiting cholinesterase activities in addition to suppressing oxidative-stress-induced neurodegeneration.

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved 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: 2017-5-1
Accepted: 2017-12-15
Published Online: 2018-2-1
Published in Print: 2018-3-28

©2018 Walter de Gruyter GmbH, Berlin/Boston

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