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Cranberry juice consumption ameliorates endothelial dysfunction during estrogen deficiency: balance between NO and ROS
Author(s) -
YUNG Lai Ming,
Wong WT,
Tian XY,
Leung FP,
Chen ZY,
Yao XQ,
Vanhoutte PM,
Huang Y
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1149.3
Subject(s) - enos , endocrinology , endothelial dysfunction , medicine , nitrotyrosine , chemistry , oxidative stress , angiotensin ii , nitric oxide , estrogen , nitric oxide synthase , receptor
This study examine whether consumption of cranberry juice could ameliorate endothelial dysfunction in estrogen deficiency. Vascular reactivity in aortas were studied in organ baths; protein levels of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS, angiotensin converting enzyme (ACE), angiotensin II type 1 (AT1R) and type 2 receptors (AT2R), gp91phox and nitrotyrosine were detected by Western blot. Angiotensin II level was detected by immunohistochemical staining. Relaxations were impaired in OVX rats; which was prevented by AT1R blocker. Cranberry juice consumption ameliorated such endothelial dysfunction. Phenylephrine‐induced tension was higher in OVX rats, which was attenuated upon juice treatment. Our results showed cranberry juice consumption in OVX rats (i) increased p‐eNOS level; (ii) restored protein expressions of ACE, AT1R, gp91phox and nitrotyrosine; (iii) restored angiotensin II level in the aorta. These suggest chronic oral administration of cranberry juice during estrogen deficiency augments bioavailability of NO, due to a reduced level of AT1R‐mediated oxidative stress.