Abstract
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), Fe3+-reducing, and Cu2+-reducing assays. The Fe2+-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 Cu2+- and Fe3+-reducing levels. In the PTIO•-scavenging assay, its IC50 values varied with pH. In the Fe2+-binding reaction, (+) taxifolin was found to yield a green solution with two UV-Vis absorbance peaks: λmax = 433 nm (ε =5.2 × 102 L mol−1 cm −1) and λmax = 721 nm (ε = 5.1 × 102 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 Fe2+.
Highlights
Antioxidant supplementation has been suggested as a means to reduce the DNA damage and relieve oxidative stress during the expansion and proliferation of bone marrow-derived mesenchymal stem cells [1]
The results indicated that (+) taxifolin (3.3–328.7 μM) had no effect on proliferation and no toxic effect on normal MSCs without OH-treatment (Additional file 1: Figure S1)
These results align with the previous findings that (+) taxifolin could be an apparent exception that could efficiently inhibit the Fenton reaction and superoxide radical formation [25, 26] while being completely nonphototoxic, unlike its analogue quercetin [13, 27]
Summary
Antioxidant supplementation has been suggested as a means to reduce the DNA damage and relieve oxidative stress during the expansion and proliferation of bone marrow-derived mesenchymal stem cells (bmMSCs) [1]. From the perspective of free radical biology, plants encounter serious oxidative stress from strong UV-Vis light, atmospheric ROS, temperature changes, and the processes of oxygen consumption for photosynthesis. Some plants, such as pine, have what could be considered a strong vital force and a long history of survival. They have successfully resisted oxidation from complicated ecological environments and may serve as a library of efficient phenolic antioxidants [3]
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