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acrolein/inflammation
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Attenuation of mouse somatic and emotional inflammatory pain by hydralazine through scavenging acrolein and inhibiting neuronal activation.
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BACKGROUND
Acrolein signaling is important during spinal cord injury; whether it is involved in somatic and emotional pain is not clear. Hydralazine is a potent antihypertensive drug and can scavenge acrolein efficiently.
OBJECTIVE
We hypothesized that hydralazine decreases spinal level acrolein and
Acrolein exposure suppresses antigen-induced pulmonary inflammation.
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BACKGROUND
Adverse health effects of tobacco smoke arise partly from its influence on innate and adaptive immune responses, leading to impaired innate immunity and host defense. The impact of smoking on allergic asthma remains unclear, with various reports demonstrating that cigarette smoke enhances
Bronchial responsiveness and inflammation in guinea pigs exposed to acrolein.
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Bronchial hyperresponsiveness can be produced experimentally after inhalation of numerous nonimmunospecific stimuli; our objective was to determine whether acrolein, a component of cigarette smoke, could increase bronchial reactivity to intravenously administered acetylcholine in guinea pigs.
[Interventions of enalapril on airway inflammation in rat models induced by acrolein].
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OBJECTIVE
To observe the effect of enalapril on airway inflammation in rat models induced by inhaling acrolein and to explore its mechanism.
METHODS
Twenty-four Sprague-Dawley rats were randomly divided into 4 groups (n = 6): 1) control group (inhaled 0.9% normal saline for 3 hours, twice every
Acrolein induces inflammatory response underlying endothelial dysfunction: a risk factor for atherosclerosis.
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Endothelial dysfunction by proinflammatory stimuli represents an important link between risk factors and the pathologic mechanisms underlying atherosclerosis. Thus, control of the inflammatory status of endothelial cells is crucial to limiting the disease. Tobacco smoking induces inflammatory
The role of T cells in the regulation of acrolein-induced pulmonary inflammation and epithelial-cell pathology.
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Exposure to acrolein in the ambient air in urban environments represents a considerable hazard to human health. Acrolein exposure causes airway inflammation, accumulation of monocytes, macrophages, and lymphocytes in the interstitium, mucous-cell metaplasia, and airspace enlargement. Currently, the
Acrolein-induced inflammatory signaling in vascular smooth muscle cells requires activation of serum response factor (SRF) and NFκB.
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BACKGROUND
Modulation of inflammatory signaling has been elucidated in several disease models. Acrolein, an environmental pollutant, has been linked to diseases such as atherosclerosis and to the inflammatory process involving nuclear factor κB (NFκB). Serum response factor (SRF), a transcription
Inhalation of the reactive aldehyde acrolein promotes antigen sensitization to ovalbumin and enhances neutrophilic inflammation.
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Acrolein (ACR), an α,β-unsaturated aldehyde and a major component of tobacco smoke, is a highly reactive electrophilic respiratory irritant implicated in asthma pathogenesis and severity. However, few studies have directly investigated the influence of ACR exposure on allergen sensitization and
Monocyte inflammation augments acrolein-induced Muc5ac expression in mouse lung.
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Acrolein, an unsaturated aldehyde found in smog and tobacco smoke, can induce airway hyperreactivity, inflammation, and mucus hypersecretion. To determine whether changes in steady-state mucin gene expression (Muc2 and Muc5ac) are associated with inflammatory cell accumulation and neutrophil
Effect of sildenafil on acrolein-induced airway inflammation and mucus production in rats.
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Airway inflammation with mucus overproduction is a distinguishing pathophysiological feature of many chronic respiratory diseases. Phosphodiesterase (PDE) inhibitors have shown anti-inflammatory properties. In the present study, the effect of sildenafil, a potent inhibitor of PDE5 that selectively
Contribution of PPARγ in modulation of acrolein-induced inflammatory signaling in gp91phox knock-out mice.
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Oxidative stress and inflammation are major contributors to acrolein toxicity. Peroxisome proliferator activated receptor gamma (PPARγ) has antioxidant and anti-inflammatory effects. We investigated the contribution of PPARγ ligand GW1929 to the attenuation of oxidative stress in acrolein-induced
A Potential Role for Acrolein in Neutrophil-Mediated Chronic Inflammation.
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Neutrophils (PMNs) are key mediators of inflammatory processes throughout the body. In this study, we investigated the role of acrolein, a highly reactive aldehyde that is ubiquitously present in the environment and produced endogenously at sites of inflammation, in mediating PMN-mediated
Acrolein inhalation suppresses lipopolysaccharide-induced inflammatory cytokine production but does not affect acute airways neutrophilia.
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Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of
Inflammatory effects of acrolein, crotonaldehyde and hexanal vapors on human primary bronchial epithelial cells cultured at air-liquid interface.
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The cytotoxicity of aldehydes was studied using human primary bronchial epithelial cells (PBEC) cultured at the air-liquid interface (ALI) or under submerged conditions. PBEC were exposed for 30min via the air phase to acrolein (0.1-1mg/m3), crotonaldehyde (1.5-15mg/m3) or hexanal (22-221mg/m3) or
Inflammatory and cytotoxic effects of acrolein, nicotine, acetylaldehyde and cigarette smoke extract on human nasal epithelial cells.
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BACKGROUND
Cigarette smoke induces a pro-inflammatory response in airway epithelial cells but it is not clear which of the various chemicals contained within cigarette smoke (CS) should be regarded as predominantly responsible for these effects. We hypothesised that acrolein, nicotine and
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