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. 2021 Mar 16;10(3):467. doi: 10.3390/antiox10030467

Table 2.

Summary of cellular or molecular mechanisms underlying the biological effects of (−)-epicatechin as well as (+)-taxifolin and/or (−)-taxifolin.

Cellular or Molecular Mechanisms (−)-Epicatechin (+)-Taxifolin and/or (−)-Taxifolin
Chelation of Fe2+, Cu2+, Zn2+ [107] [108]
ROS scavenging [105,106] [108]
Alterations of iron metabolism [60,72] [40,83]
Activation of antioxidant enzymes (SOD, CAT, or GPx) [181,182] [76,183]
Reduction of NOX or XO [61,62,88,109,182,184] [96,109,110]
Elevation of endothelial NO [38,61,62,68,181] [66]
Reduction of inducible NOS-produced NO [87,90,131] [90,129,130,131,185]
Arginase inhibition [58,132,133] [133]
Reduction of ACE [160,161] [65,186,187]
Nrf2 induction [61,121] [76,121,122]
NFκB reduction [87,137,188] [140]
Inflammasome reduction [141,142]

Abbreviations: ACE, angiotensin-converting enzyme; CAT, catalase; GPx, glutathione peroxidase; NF-κB, nuclear factor-κB; NO, nitric oxide; NOS, nitric oxide synthase; NOX, nicotinamide adenine dinucleotide phosphate oxidase; Nrf2, nuclear factor erythroid-2 related factor 2; ROS, reactive oxygen species; SOD, superoxiddismutase; XO, xanthine oxidase.