Delphinidine (delph), an anthocyanin with the same pharmacological pro¿ le
than the total extract of red wine polyphenol, induces vasodilatation and possess
anti-apoptotic property in endothelial cells (ECs) by mechanism involving nitric
oxide (NO). The later can regulate mitochondrial (mt) function. However, the
link between NO, mitochondria and the upstream target of delph including the
alpha isoform of the estrogen receptor (ERa) has never been assessed and is
the aim of the present study. For this purpose, the effects of delph (3.10-5 M) and the ERa agonist propylpyrazole triol (PPT, 10-5 M) were conducted at two
time points, 10min and 48h, on mt respiration (R) by oxygraphy and on respi-
ratory chain complexes activities by spectrophotometry in Eahy926 ECs. NO
production was assessed by electron paramagnetic resonance at the early time.
These experiments were performed with or without the ER antagonist, fulves-
trant (fulv, 3.10-5 M), or the NO synthase inhibitor, L-nitro-arginine (L-NA,
10-4 M). As expected, delph and PPT induced an early increase of NO that
was prevented by fulv. Delph time-dependently increased basal R and maximal
R capacity but not the non-phosphorylative R by a mechanism insensitive to
fulv but sensitive to L-NA. PPT did not affect basal and non-phosphorylative
R but increased the maximal R capacity by a mechanism sensitive to fulv and
L-NA. These effects were associated with increased cytochrome c oxidase acti-
vity. These data highlight the implication of both NO and cytochrome c oxidase
activity on the modulation of mt R in response to delph and PPT in ECs. The
lack of effect of ER blockade on the increase of mt R by delph supports the
involvement of ER-independent mechanism although this receptor is implicated
at the early increase of NO production. Thus, this study suggests a probable role
of mitochondria in the effect of polyphenol in the regulation of endothelial func-
tion including vasodilatation and endothelial integrity.