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Antioxydant treatment prevents endothelial dysfunction and alteration of the eNOS pathway associated with severe dyslipidemia in mouse cerebral arteries
Author(s) -
Drouin Annick,
Thorin Eric
Publication year - 2009
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.23.1_supplement.628.7
Subject(s) - enos , medicine , endocrinology , endothelial dysfunction , cerebral arteries , catechin , endothelium , chemistry , apolipoprotein b , nitric oxide , cholesterol , biochemistry , antioxidant , nitric oxide synthase , polyphenol
Endothelial dysfunction observed in cardiovascular diseases has been linked with an excess in free radical formation. We hypothesized that a chronic treatment with the antioxydant catechin would preserve the endothelium by maintaining eNOS function in dyslipidemic mice (DL). DL (C57Bl/6‐LDLR −/− ;ApoB +/+ ) 3 months‐old (m/o) male mice were treated with catechin (30 mg/kg/day) for 3 months. C57Bl/6 (WT) were used as controls. Endothelium‐dependent dilations to acetylcholine (EDD; % max diameter) were recorded in pressurized cerebral arteries. Results are mean±SEM of n = 6 mice. Myogenic tone (MT) increased in DL at 3 and 6 m/o (from 14±5% and 22±4% in WT, to 44±4% and 48±5% in DL; p<.05) but was restored by catechin (29±4%). eNOS inhibition with N‐nitro‐L‐arginine (L‐NNA) increased MT at both ages in WT (p<.05) but not in DL (43±6%, 34±4%, 58±6% and 52±5%, respectively). EDD was reduced at 3 and further at 6 months in DL compared to WT (26±2%, 17±2%, 45±6% and 38±4%, respectively; p<.05). L‐NNA reduced EDD in 3 and 6 m/o WT and in 3 m/o DL (24±2, 20±4% and 13±4%, respectively; p<0.5) but not in 6 m/o DL (18±2%). Catechin improved EDD in DL (31±3%; p<0.5) and restored eNOS function: L‐NNA reduced EDD (9±1%; p<.05) and increased MT (44±4%; p<.05). In conclusion, chronic treatment with catechin limits endothelial dysfunction due to its protective effect on the eNOS pathway in DL mouse cerebral arteries. This work is supported by CIHR.