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Dihydromyricetin attenuates platelet hyperactivity in HFD/STZ-induced diabetic mice by inhibiting intraplatelet ROS

Fenglin Song1,2, Huafang Ding1, Yun Chen1

  • 1School of Food Science, Guangdong Pharmaceutical University, Zhongshan, Guangdong Province, 528458, China. zhenyuchen@cuhk.edu.hk.

Food & Function
|May 26, 2026
PubMed

Insights

Dihydromyricetin (DHM) supplementation reduced platelet hyperactivity and thrombus formation in diabetic mice by suppressing oxidative stress. This suggests DHM may help prevent cardiovascular complications associated with type 2 diabetes mellitus (T2DM).

Area of Science:

  • Cardiovascular Science
  • Nutritional Science
  • Pharmacology

Background:

  • Platelet hyperactivity is a key factor in cardiovascular complications of type 2 diabetes mellitus (T2DM).
  • Dihydromyricetin (DHM), a natural polyphenol, shows potential in inhibiting platelet activation.
  • Understanding DHM's in vivo effects on diabetic platelet function is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the mechanisms and in vivo effects of dietary DHM on platelet hyperactivity in a mouse model of T2DM.
  • To assess DHM's impact on platelet activation markers, oxidative stress, and thrombosis in diabetic conditions.

Main Methods:

  • A T2DM mouse model was induced using a high-fat diet (HFD) and streptozotocin (STZ).
  • Mice received dietary DHM supplementation (500 or 1000 mg kg⁻¹) for eight weeks.
  • Flow cytometry, platelet aggregation assays, plasma marker analysis, and pulmonary embolism models were employed. Molecular docking was used to predict binding interactions.

Main Results:

  • DHM significantly reduced platelet activation markers (CD62P, CD63, CD40L, αIIbβ3), intraplatelet ROS, and platelet aggregation/ATP secretion.
  • Plasma levels of soluble P-selectin, platelet factor 4, thromboxane B2, and 8-iso-prostaglandin F2α were decreased by DHM.
  • DHM delayed pulmonary embolism formation without affecting bleeding time and showed potential binding interactions with key platelet proteins.

Conclusions:

  • Dietary DHM effectively attenuates platelet hyperactivity and thrombus formation in T2DM mice, primarily by reducing oxidative stress.
  • DHM demonstrates potential as a natural therapeutic agent for mitigating diabetic cardiovascular complications.
  • Further research into DHM's cardioprotective mechanisms in diabetes is warranted.

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