Stroke · 2004
Concurrent treatment with renin-angiotensin system blockers and acetylsalicylic acid reduces nuclear factor kappaB activation and C-reactive protein expression in human carotid artery plaques.
Клиническое исследованиеКонтролируемое клиническое исследованиеСтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Sattler Katherine J E, Woodrum Julie E, Galili Offer, Olson Monica, Samee Saquib, Meyer Fredric B, Zhu Xiang-Yang, Lerman Lilach O, Lerman Amir
Аннотация
BACKGROUND AND PURPOSE: The local renin-angiotensin system (RAS) and cyclooxygenase-2 contribute to the activation of nuclear factor kappaB (NFkappaB) and C-reactive protein (CRP). We hypothesized that the combination of RAS blockers (RASb) and ASA reduces NFkappaB and CRP within atherosclerotic plaques.
METHODS: Patients undergoing carotid endarterectomy were divided into groups according to treatment (RASb-acetylsalicylic acid [ASA], ASA, RASb, and control). The expression of NFkappaB, CRP, and CD40L was analyzed through Western blots in the obtained plaques.
RESULTS: Plaques from patients treated with the combination of RASb and ASA showed lower expression of NFkappaB (25.4+/-9.8 densitometric units [DU]) than those of the control group (57.6+/-13.2 DU, P=0.03) as well as lower expression of CRP (20.9+/-9.6 DU) than those of the other treatment groups (ASA 86.1+/-13 DU, RASb 88.4+/-31 DU, controls 67.8+/-18.6, P=0.004). A negative expression of NFkappaB was associated with a reduced incidence of symptoms compared with a positive expression (5/33 [15.1%] versus 14/35 [40%], P=0.031).
CONCLUSIONS: The combined treatment with RASb and ASA decreases the expression of inflammatory markers in atherosclerosis in humans. This study supports the role of the local RAS and cyclooxygenase-2 in the progression of atherosclerosis.
METHODS: Patients undergoing carotid endarterectomy were divided into groups according to treatment (RASb-acetylsalicylic acid [ASA], ASA, RASb, and control). The expression of NFkappaB, CRP, and CD40L was analyzed through Western blots in the obtained plaques.
RESULTS: Plaques from patients treated with the combination of RASb and ASA showed lower expression of NFkappaB (25.4+/-9.8 densitometric units [DU]) than those of the control group (57.6+/-13.2 DU, P=0.03) as well as lower expression of CRP (20.9+/-9.6 DU) than those of the other treatment groups (ASA 86.1+/-13 DU, RASb 88.4+/-31 DU, controls 67.8+/-18.6, P=0.004). A negative expression of NFkappaB was associated with a reduced incidence of symptoms compared with a positive expression (5/33 [15.1%] versus 14/35 [40%], P=0.031).
CONCLUSIONS: The combined treatment with RASb and ASA decreases the expression of inflammatory markers in atherosclerosis in humans. This study supports the role of the local RAS and cyclooxygenase-2 in the progression of atherosclerosis.