Protective Effects of Dihydromyricetin against •OH-Induced Mesenchymal Stem Cells Damage and Mechanistic Chemistry
As a natural flavonoid inAmpelopsis grossedentata, dihydromyricetin (DHM,2R,3R-3,5,7,3′,4′,5′-hexahydroxy-2,3-dihydroflavonol) was observed to increase the viability of •OH-treated mesenchymal stem cells using a MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl] assay and flow cytometry analysis. This protective effect indicates DHM may be a beneficial agent for cell transplantation therapy. Mechanistic chemistry studies indicated that compared with myricetin, DHM was less effective at ABTS+• (2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid radical) scavenging and reducing Cu2+, and had higher •O2−and DPPH• (1,1-diphenyl-2-picrylhydrazyl radical) scavenging activities. Additionally, DHM could also chelate Fe2+to give an absorption maximum at 589 nm. Hence, such protective effect of DHM may arise from its antioxidant activities which are thought to occur via direct radical-scavenging and Fe2+-chelation. Direct radical-scavenging involves an electron transfer (ET) pathway. The hydrogenation of the 2,3-double bond is hypothesized to reduce the ET process by blocking the formation of a larger π-π conjugative system. The glycosidation of the 3–OH in myricitrin is assumed to sterically hinder atom transfer in the •O2−and DPPH• radical-scavenging processes. In DHM, the Fe2+-chelating effect can actually be attributed to the 5,3′,4′,5′–OH and 4–C=O groups, and the 3–OH group itself can neither scavenge radicals nor chelate metal.Keywords:dihydromyricetin;mesenchymal stem cells;antioxidant mechanisms;hydroxyl radical-induced;Fe2+-chelation;3–OH group;2,3-double bond;electron transfer (ET) pathway
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