Blueberry anthocyanin extract inhibits platelet activation and FUNDC1-mediated mitophagy in type 2 diabetes mellitus via AMPK pathway.

HPLC analysis was employed to identify the chemical compositions in BAE. Delphinidin, cyanidin, peonidin, and malvidin were detected in BAE.After establishment of the T2DM mice model, BAE and metformin were treated. Body weight, fasting blood glucose level and glucose tolerance were monitored, followed by detection of β-TG, PF4, CD62p, mitophagy markers. Both BAE and metformin implement reduced the body weight and fasting blood glucose level, and improved glucose tolerance of T2DM mice. BAE implement significantly reduced the β-TG, PF4 and CD62p levels in T2DM mice. FUNDC1, LC3II/LC3I, Pink1, and Parkin protein levels were both significantly elevated in T2DM mice, while Tomm20 expression was remarkedly reduced. BAE implement effectively reversed the FUNDC1, LC3II/LC3I, Pink1, and other relevant markers in T2DM mice.The effect of AMPK pathway involved in the BAE for T2DM treatment was explored. STZ treatment significantly decreased the phospho-AMPK level, while BAE administration reversed the effects of STZ on phospho-AMPK level in mice. Compound C implement effectively abolished the effects of BAE on the expression of platelet activation and mitophagy markers.This study suggests that BAE ameliorates T2DM through inhibiting platelet activation and FUNDC1-mediated platelet mitophagy via the AMPK pathway.