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<p>The aim of this study was to evaluate the total content of flavonoids and phenols, in vitro antioxidant and cytoprotective effects of <i>Sclerocarya birrea</i> fruit exocarp extracts. The fruit exocarp was extracted sequentially in Hexane, Chloroform, Ethyl acetate, and Methanol and the antioxidant properties were evaluated using in vitro antioxidant assays and cytoprotective effects against H<sub>2</sub>O<sub>2</sub>-induced cell death using HeLa cells. Molecular docking using Autodock 4.2.6 was used to assess the binding interactions of <i>Sclerocarya birrea</i> compounds to the antioxidant enzymes. The total flavonoid and total phenolic contents were in the order Methanol &gt; Ethyl acetate &gt; Chloroform &gt; Hexane (<i>P</i> &lt; 0.05) of <i>Sclerocarya birrea</i> fruit exocarp extracts. The antioxidant properties using DPPH, ABTS, and Ferric reducing antioxidant power, and total antioxidant capacity assays revealed significantly higher (<i>P</i> &lt; 0.05) antioxidant activity in the Methanol &gt; Ethyl acetate &gt; Chloroform &gt; Hexane. Using WST-1 assay, H<sub>2</sub>O<sub>2</sub>-induced cell loss was effectively reduced by preincubating HeLa cells with Ethyl acetate &gt; Methanol &gt; Chloroform &gt; Hexane (<i>P</i> &lt; 0.05) extracts. Methanol and Ethyl acetate extracts also significantly increased (<i>P</i> &lt; 0.05) the activities of Superoxide dismutase, Catalase and reduced Glutathione. Amongst the identified compounds, Myricetin 3-o-α- rhamsoside (C8) emerged as the best compound to bind to both SOD and CAT with binding energies of − 9.1 and − 8.8&#xa0;kcal/mol respectively. C8 formed hydrogen bonds and electrostatic interactions with SOD and CAT to act as an agonist. Our findings suggest that Methanol and Ethyl acetate <i>Sclerocarya birrea</i> fruit exocarp extracts improved antioxidant capacity and thus have the potential to be developed into antioxidant products that will alleviate oxidative stress linked diseases.</p>

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Flavonoids and phenols of Sclerocarya birrea fruit exocarp extracts differentially modulating antioxidant activities

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月18日

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  • Phazha Bushe Baeti,
  • Keagile Bati,
  • Phenyo Donald Brown,
  • Runner Majinda,
  • Kabo Masisi,
  • Goabaone Gaobotse,
  • Tebogo Elvis Kwape

摘要

The aim of this study was to evaluate the total content of flavonoids and phenols, in vitro antioxidant and cytoprotective effects of Sclerocarya birrea fruit exocarp extracts. The fruit exocarp was extracted sequentially in Hexane, Chloroform, Ethyl acetate, and Methanol and the antioxidant properties were evaluated using in vitro antioxidant assays and cytoprotective effects against H2O2-induced cell death using HeLa cells. Molecular docking using Autodock 4.2.6 was used to assess the binding interactions of Sclerocarya birrea compounds to the antioxidant enzymes. The total flavonoid and total phenolic contents were in the order Methanol > Ethyl acetate > Chloroform > Hexane (P < 0.05) of Sclerocarya birrea fruit exocarp extracts. The antioxidant properties using DPPH, ABTS, and Ferric reducing antioxidant power, and total antioxidant capacity assays revealed significantly higher (P < 0.05) antioxidant activity in the Methanol > Ethyl acetate > Chloroform > Hexane. Using WST-1 assay, H2O2-induced cell loss was effectively reduced by preincubating HeLa cells with Ethyl acetate > Methanol > Chloroform > Hexane (P < 0.05) extracts. Methanol and Ethyl acetate extracts also significantly increased (P < 0.05) the activities of Superoxide dismutase, Catalase and reduced Glutathione. Amongst the identified compounds, Myricetin 3-o-α- rhamsoside (C8) emerged as the best compound to bind to both SOD and CAT with binding energies of − 9.1 and − 8.8 kcal/mol respectively. C8 formed hydrogen bonds and electrostatic interactions with SOD and CAT to act as an agonist. Our findings suggest that Methanol and Ethyl acetate Sclerocarya birrea fruit exocarp extracts improved antioxidant capacity and thus have the potential to be developed into antioxidant products that will alleviate oxidative stress linked diseases.