human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['NAD(P)H oxidase and COX-1 participate in vascular damage induced by angiotensin II. We investigated the effect of rosuvastatin on endothelial dysfunction, vascular remodelling, changes in extracellular matrix components and mechanical properties of small mesenteric arteries from angiotensin II-infused rats.', 'Male rats received angiotensin II (120 ng·kg⁻¹ ·min⁻¹ , subcutaneously) for 14 days with or without rosuvastatin (10 mg·kg⁻¹ ·day⁻¹ , oral gavage) or vehicle. Vascular functions and morphological parameters were assessed by pressurized myography.', 'In angiotensin II-infused rats, ACh-induced relaxation was attenuated compared with controls, less sensitive to L-NAME, enhanced by SC-560 (COX-1 inhibitor) or SQ-29548 (prostanoid TP receptor antagonist), and normalized by the antioxidant ascorbic acid or NAD(P)H oxidase inhibitors. After rosuvastatin, relaxations to ACh were normalized, fully sensitive to L-NAME, and no longer affected by SC-560, SQ-29548 or NAD(P)H oxidase inhibitors. Angiotensin II enhanced intravascular superoxide generation, eutrophic remodelling, collagen and fibronectin depositions, and decreased elastin content, resulting in increased vessel stiffness. All these changes were prevented by rosuvastatin. Angiotensin II increased phosphorylation of NAD(P)H oxidase subunit p47phox and its binding to subunit p67phox, effects inhibited by rosuvastatin. Rosuvastatin down-regulated vascular Nox4/NAD(P)H isoform and COX-1 expression, attenuated the vascular release of 6-keto-PGF1α , and enhanced copper/zinc-superoxide dismutase expression.'] Does rosuvastatin prevent angiotensin II-induced vascular changes by inhibition of NAD ( P ) H oxidase and COX-1?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['NAD(P)H oxidase and COX-1 participate in vascular damage induced by angiotensin II. We investigated the effect of rosuvastatin on endothelial dysfunction, vascular remodelling, changes in extracellular matrix components and mechanical properties of small mesenteric arteries from angiotensin II-infused rats.', 'Male rats received angiotensin II (120 ng·kg⁻¹ ·min⁻¹ , subcutaneously) for 14 days with or without rosuvastatin (10 mg·kg⁻¹ ·day⁻¹ , oral gavage) or vehicle. Vascular functions and morphological parameters were assessed by pressurized myography.', 'In angiotensin II-infused rats, ACh-induced relaxation was attenuated compared with controls, less sensitive to L-NAME, enhanced by SC-560 (COX-1 inhibitor) or SQ-29548 (prostanoid TP receptor antagonist), and normalized by the antioxidant ascorbic acid or NAD(P)H oxidase inhibitors. After rosuvastatin, relaxations to ACh were normalized, fully sensitive to L-NAME, and no longer affected by SC-560, SQ-29548 or NAD(P)H oxidase inhibitors. Angiotensin II enhanced intravascular superoxide generation, eutrophic remodelling, collagen and fibronectin depositions, and decreased elastin content, resulting in increased vessel stiffness. All these changes were prevented by rosuvastatin. Angiotensin II increased phosphorylation of NAD(P)H oxidase subunit p47phox and its binding to subunit p67phox, effects inhibited by rosuvastatin. Rosuvastatin down-regulated vascular Nox4/NAD(P)H isoform and COX-1 expression, attenuated the vascular release of 6-keto-PGF1α , and enhanced copper/zinc-superoxide dismutase expression.'] Does rosuvastatin prevent angiotensin II-induced vascular changes by inhibition of NAD ( P ) H oxidase and COX-1?
OUTPUT:
