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Flavonoids from Inula Britannica L. inhibits injury‐induced neointimal hyperplasia through suppressing oxidative stress generation
Author(s) -
Zhang HongBing,
Wen JinKun,
Wang YanYan,
Zheng Bin,
Han Mei
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.lb229
Subject(s) - neointimal hyperplasia , atorvastatin , oxidative stress , medicine , hyperplasia , restenosis , quercetin , endocrinology , urology , chemistry , stent , antioxidant , biochemistry
The total flavonoid extracts (TFE) were prepared from Inula Britannica L., containing 45.5% quercetin, 25.85% luteolin, 12.96% 6‐methoxyluteolin, 4.33% spinacetin and 1.85% isorhamnetin. To explore the effect of TFE on neoinimal hyperplasia induced by balloon injury, the rats administered orally TFE at doses of 12.5, 25, and 50mg/kg/d by gastric gavage from 3 days before balloon injury to 14 days after the injury, respectively. We found that the rats treated with high dose of TFE (50 mg) showed a reduced neointimal hyperplasia, and the ratio of intima (I) to media (M) area (I/M) of balloon injured‐carotid arteries was significantly reduced by over 70% after TFE treatment, compared with model group. The inhibitory effect of TFE (50 mg) on neointimal hyperplasia was almost consistent with Atorvastatin, as a positive control. The plasma SOD activity was obviously increased in TFE (50 mg)‐treated group (P < 0.01), meanwhile, plasma MDA production was markedly decreased (P < 0.05). At 14 days after balloon injury, the neointimal and medial layer of the carotid arteries showed an increase in O2? production. TFE (50 mg) significantly prevented the injury‐induced O2? production, and inhibited the injury‐induced p47phox expression in carotid arteries. These results suggest that the TFE inhibits the neointimal hyperplasia induced by balloon injury through suppressing oxidative stress generation.