The mechanism of (+) taxifolin’s protective antioxidant effect for •OH-treated bone marrow-derived mesenchymal stem cells

The natural dihydroflavonol (+) taxifolin was investigated for its protective effect on Fenton reagent-treated bone marrow-derived mesenchymal stem cells (bmMSCs). Various antioxidant assays were used to determine the possible mechanism. These included •OH-scavenging, 2-phenyl-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide radical-scavenging (PTIO•-scavenging), 1, 1-diphenyl-2-picryl-hydrazl radical-scavenging (DPPH•-scavenging), 2, 2′-azino-bis (3-ethylbenzo-thiazoline-6-sulfonic acid) radical-scavenging (ABTS(+)•-scavenging), Fe(3+)-reducing, and Cu(2+)-reducing assays. The Fe(2+)-binding reaction was also investigated using UV-Vis spectra. The results revealed that cell viability was fully restored, even increasing to 142.9 ± 9.3% after treatment with (+) taxifolin. In the antioxidant assays, (+) taxifolin was observed to efficiently scavenge •OH, DPPH• and ABTS(+)• radicals, and to increase the relative Cu(2+)- and Fe(3+)-reducing levels. In the PTIO•-scavenging assay, its IC(50) values varied with pH. In the Fe(2+)-binding reaction, (+) taxifolin was found to yield a green solution with two UV-Vis absorbance peaks: λ(max) = 433 nm (ε =5.2 × 10(2) L mol(−1) cm (−1)) and λ(max) = 721 nm (ε = 5.1 × 10(2) L mol(−1) cm (−1)). These results indicate that (+) taxifolin can act as an effective •OH-scavenger, protecting bmMSCs from •OH-induced damage. Its •OH-scavenging action consists of direct and indirect antioxidant effects. Direct antioxidation occurs via multiple pathways, including ET, PCET or HAT. Indirect antioxidation involves binding to Fe(2+). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s11658-017-0066-9) contains supplementary material, which is available to authorized users.