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An In Vitro and Molecular Informatics Study to Evaluate the Antioxidative and β‐hydroxy‐β‐methylglutaryl‐CoA Reductase Inhibitory Property of Ficus virens Ait
Author(s) -
Iqbal Danish,
Khan M. Salman,
Khan Mohd. S.,
Ahmad Saheem,
Srivastava Ashwini K.
Publication year - 2014
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5077
Subject(s) - antioxidant , quinic acid , oxidative stress , chemistry , biochemistry , reductase , bark (sound) , traditional medicine , in vitro , phytochemical , enzyme , biology , medicine , ecology
The present study is initially intended to evaluate antioxidant and β‐hydroxy‐β‐methylglutaryl‐CoA reductase (HMGR) inhibitory property of Ficus virens Ait., first by in vitro analyses followed by a corroboratory molecular informatics study. Our results show that of all the sequentially extracted fraction of F . virens bark and leaves extract, F . virens bark methanol extract exhibits strong radical scavenging, antioxidant and oxidative DNA damage protective activity, which is well correlated with its total phenolic content. In addition, F . virens bark methanol extract, which is non‐cytotoxic, significantly and non‐covalently inhibit the HMGR activity (IC 50 = 3.45 ± 0.45 µg/ml) in comparison with other extracts. The mechanistic aspect of this inhibition activity is authenticated by molecular docking study of bioactive compounds as revealed from gas chromatography–mass spectrometry data, with HMGR. The analysis for the first time indicates that quinic acid (ΔG: −8.11 kcal/mol) and paravastatin (ΔG: −8.22 kcal/mol) exhibit almost same binding energy, while other compounds also showed good binding energy, suggesting that quinic acid alone or in combination with other major bioactive compound is probably responsible for HMGR inhibitory property of the extract and plausibly can be used in in vivo system for the management, prevention, and alleviation of hypercholesterolemia as well as hypercholesterolemia‐induced oxidative stress. Copyright © 2013 John Wiley & Sons, Ltd.