Dihydromyricetin Acts as a Potential Redox Balance Mediator in Cancer Chemoprevention

Abstract

Dihydromyricetin (DHM) is a flavonoid extracted from the leaves and stems of the edible plant Ampelopsis grossedentata that has been used for Chinese Traditional Medicine. It has attracted considerable attention from consumers due to its beneficial properties including anticancer, antioxidative, and anti-inflammatory activities. Continuous oxidative stress caused by intracellular redox imbalance can lead to chronic inflammation, which is intimately associated with the initiation, promotion, and progression of cancer. DHM is considered a potential redox regulator for chronic disease prevention, and its biological activities are abundantly evaluated by using diverse cell and animal models. However, clinical investigations are still scanty. This review summarizes the current potential chemopreventive effects of DHM, including its properties such as anticancer, antioxidative, and anti-inflammatory activities, and further discusses the underlying molecular mechanisms of DHM in cancer chemoprevention by targeting redox balance and influencing the gut microbiota.

A multifaceted review on dihydromyricetin resources, extraction, bioavailability, biotransformation, bioactivities, and food applications with future perspectives to maximize its value

“…DMY is a white needle-like crystal obtained from ethanol with very poor water-solubility and stability as well as powerful antioxidative activity [19]. DMY with 2-phenylchromogenone as the core structure belongs to the class IV based on the biopharmaceutical classification system (BCS) due to its low solubility and permeability [7].…”

“…DMY exhibits broad anticancer activities in multiple cancer cells and animal models of cancer. With excellent antioxidant and anti‐inflammatory activities, DMY played a significant role in tumor chemoprevention by eliminating reactive oxygen species, influencing gut microbiota, and regulating signaling pathways in cells [19].…”

“…Compared to typical antithrombotic and antiplatelet drugs, DMY hindered thrombus formation by preventing aggregation of platelet and generation of fibrin in the mouse model of laser‐induced thrombosis. For the mechanism of action, DMY suppressed mitogen‐activated protein kinase (MAPK) and attenuated Ca 2 + increase in platelets and endothelial cells [19].…”

“…In contrast, IC 50 values of the DMY in the DPPH and ABTS assays were determined at 7 and 2 μ M, respectively [21]. EC 50 values of DMY for scavenging DPPH, ABTS, H 2 O 2 , and O 2 radicals were at 8.18, 5.32, 7.95, and 7.79 μ g/mL, respectively [19]. IC 50 of DMY in the DPPH assay was estimated at 3.24 μ g/mL and the oxygen radical absorbance capacity (ORAC) value of DMY was close to 4000 μ moL/g [23].…”

“…Among these factors, pH plays a critical role in the stability of DMY. DMY is more stable in the acidic pH range of 1.0‐5.0, while readily oxidized and significantly degraded in the alkaline pH range, especially at 6.0‐8.0 [19]. The gastrointestinal (GI) stability study indicated that DMY was stable at pH 1.2, though unstable at pH 6.8 in a simulated digestive system.…”