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smooth/antioxidant
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Effect of antioxidants on airway smooth muscle contraction: action of lipoic acid and some of its novel derivatives on guinea pig tracheal smooth muscle.
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OBJECTIVE
The aim of this study was to investigate the ability of (a) antioxidants, some related to alpha-lipoic acid (LA), (b) histone deacetylase (HDAC) inhibitors, and (c) hybrid compounds possessing both alpha-lipoic acid-derived antioxidant properties and HDAC inhibitory activity to inhibit
Glutathione peroxidase-deficient smooth muscle cells cause paracrine activation of normal smooth muscle cells via cyclophilin A.
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OBJECTIVE
Reduced activity of the antioxidant glutathione peroxidase-1 (GPx1) correlates with increased risk of cardiovascular events in patients with coronary artery disease. However, it remains unclear whether this imbalance in antioxidant capacity directly contributes to activation of vascular
Antioxidants counteract lipopolysaccharide-triggered alterations of human colonic smooth muscle cells.
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Gut dysmotility develops in individuals during and after recovering from infective acute gastroenteritis and it is apparently due to a direct effect of circulating lipopolysaccharides (LPS). This is an endotoxin with a prooxidant activity derived from gram-negative bacteria. Due to the lack of human
Redox control of vascular smooth muscle proliferation.
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Recent evidence suggests a role for reactive oxygen species in the control of vascular smooth muscle proliferation both in vitro and in vivo. Oxidative stress increases cell proliferation, mediates hormone-induced hypertrophy, and-under some circumstances-induces apoptosis. Smooth muscle cells
Cordycepin inhibits vascular smooth muscle cell proliferation.
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Percutaneous transluminal coronary angioplasty (PTCA) is a common procedure for treating atherosclerosis, but its efficacy is limited because of the occurrence of restenosis within 3-6 months after angioplasty. Restenosis is induced by the remodeling of the vessel wall and/or the accumulation of
Ligustilide inhibits vascular smooth muscle cells proliferation.
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Proliferation and migration of vascular smooth muscle cells (VSMCs) are believed to develop atherosclerosis and venous bypass graft disease. Ligustilide is widely used to treat some pathological settings such as atherosclerosis and hypertension. The aim of this study was to examine the effect of
Magnolol induces apoptosis in vascular smooth muscle.
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Magnolol, an active component extracted from Magnolia officinalis, has various pharmacological effects, including potent antioxidant activity. In the present study, we investigated the effect of magnolol on apoptosis in rat vascular smooth muscle cells (VSMCs), using
Dipyridamole: an antioxidant that promotes the proliferation of aorta smooth muscle cells.
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Smooth muscle cells from guinea pig aorta were grown in tissue culture. Dipyridamole enhanced the proliferation of these cells in culture and dipyridamole overcame the inhibitory effect of arachidonic acid on cell proliferation. Dipyridamole and the antioxidant vitamin E both increased the cloning
Antioxidant-independent ascorbate enhancement of catecholamine-induced contractions of vascular smooth muscle.
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Ascorbate reduces the oxidation rate of catecholamines and, by an independent mechanism, enhances rabbit aortic ring contractions initiated by catecholamines. The largest significantly different fractional increases in force produced by ascorbate enhancement of norepinephrine (NE), epinephrine,
Vascular smooth muscle and endothelial functions in aging.
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Aging is one of the main risk factors for the development of atherosclerosis and, therefore, for coronary artery disease. Age-associated remodeling of the vascular wall includes luminal enlargement, intimal and medial thickening, and increased vascular stiffness. As aging occurs, smooth muscle cells
Calcium antagonists and vascular smooth muscle cell reactivity.
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OBJECTIVE
To determine the mechanisms whereby calcium channel blockers (CCBs) control the reactivity of vascular smooth muscle cells (VSMCs).
BACKGROUND
Although CCBs are known to play an important role in the calcium homeostasis of VSMCs, they are suspected to exert additional effects in this cell
Effect of illuminated nifedipine, a potent antioxidant, on intestinal and vascular smooth muscles.
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1. The effects of nifedipine (Nif) and its illuminated nitroso product nitrosopine (NTP) were investigated on lipid peroxidation, KCl elevated smooth muscle tension, and ionic currents of single smooth muscle cells. 2. Illumination of Nif at 400-700 nm within 24-48 h changed it completely to a
Internal mammary artery smooth muscle cells resist migration and possess high antioxidant capacity.
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OBJECTIVE
This study investigated whether differences exist in atherogen-induced migratory behaviors and basal antioxidant enzyme capacity of vascular smooth muscle cells (VSMC) from human coronary (CA) and internal mammary (IMA) arteries.
METHODS
Migration experiments were performed using the Dunn
Release of the antioxidants ascorbate and urate from a nitrergically-innervated smooth muscle.
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1. The main object of the present study was to determine whether ascorbate, an antioxidant which has been shown to protect nitric oxide (NO) from attack by scavenger molecules, might be released from nitrergically-innervated smooth muscle; ascorbate release from the rat anococcygeus was measured by
Urokinase induces ROS production in vascular smooth muscle cells.
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Urokinase stimulates the production of superoxide radical in cultured aortal smooth muscle cells simultaneously with activation of the expression of NAD(F)H-oxidases nox1, nox4, and phox22. Antioxidant ebselen abolishes the stimulating effect of urokinase on smooth muscle cell proliferation. The
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