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monocrotaline/nécrose
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An inhibitory effect of tumor necrosis factor-alpha antagonist to gene expression in monocrotaline-induced pulmonary hypertensive rats model.
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OBJECTIVE
Tumor necrosis factor (TNF)-α is thought to contribute to pulmonary hypertension. We aimed to investigate the effect of infliximab (TNF-α antagonist) treatment on pathologic findings and gene expression in a monocrotaline-induced pulmonary hypertension rat model.
METHODS
Six-week-old male
Chymase inhibition attenuates monocrotaline-induced sinusoidal obstruction syndrome in hamsters.
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Chymase stored in mast cells activates matrix metalloproteinase (MMP)-9, which may relate to the progression of sinusoidal obstruction syndrome (SOS). We investigated the preventive effect of a chymase inhibitor, TY-51469, on monocrotaline-induced SOS in hamsters. Hamsters were orally administrated
Isoliquiritigenin Attenuates Monocrotaline-Induced Pulmonary Hypertension via Inhibition of the Inflammatory Response and PASMCs Proliferation.
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Pulmonary hypertension (PH) is a progressive and serious disease, where exacerbated inflammatory response plays a critical role. Isoliquiritigenin (ISL), an important flavonoid isolated from Glycyrrhizae radix, exhibits a wide range of pharmacological actions including anti-inflammation. Previously
Apoptosis and inflammation associated gene expressions in monocrotaline-induced pulmonary hypertensive rats after bosentan treatment.
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OBJECTIVE
Vascular wall remodeling in pulmonary hypertension can be caused by an aberration in the normal balance between proliferation and apoptosis of endothelial cell in the pulmonary artery. The objective of this study was to evaluate the effect of bosentan on apoptosis in monocrotaline
Resveratrol prevents monocrotaline-induced pulmonary hypertension in rats.
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Proliferation of pulmonary arterial smooth muscle cells, endothelial dysfunction, oxidative stress, and inflammation promotes the development of pulmonary hypertension. Resveratrol is a polyphenolic compound that exerts antioxidant and anti-inflammatory protective effects in the systemic
Role of oxidative stress, inflammation, nitric oxide and transforming growth factor-beta in the protective effect of diosgenin in monocrotaline-induced pulmonary hypertension in rats.
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Pulmonary hypertension is a progressive disease of various origins that is associated with right ventricular dysfunction. In the present study, the protective effect of diosgenin was investigated in monocrotaline-induced pulmonary hypertension in rats. Pulmonary hypertension was induced by a single
Fluoxetine inhibited extracellular matrix of pulmonary artery and inflammation of lungs in monocrotaline-treated rats.
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OBJECTIVE
To investigate the effects of the selective serotonin reuptake inhibitor (SSRI) fluoxetine on extracellular matrix (ECM) remodeling of the pulmonary artery and inflammation of the lungs in pulmonary arterial hypertension (PAH) induced by monocrotaline in rats.
METHODS
MCT-induced chronic
Anti-TNF treatment reduces rat skeletal muscle wasting in monocrotaline-induced cardiac cachexia.
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The aim was to explore efficacy of tumor necrosis factor (TNF) inhibitors in attenuating increases in anorexia and ubiquitin proteasome pathway transcripts in cardiac cachexia, a potentially lethal condition that responds poorly to current treatments. Cardiac cachexia was rapidly induced with
Chlorogenic acid suppresses monocrotaline-induced sinusoidal obstruction syndrome: The potential contribution of NFκB, Egr1, Nrf2, MAPKs and PI3K signals.
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Hepatic sinusoidal obstruction syndrome (SOS) is a highly lethal liver disease. This study aims to observe the protection and its engaged mechanism of chlorogenic acid (CGA) against monocrotaline (MCT)-induced SOS. Results of detecting liver ascites, measuring serum transaminases, liver histological
Cytotoxic carcinogeneic response to monocrotaline pyrrole.
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The cytotoxic and carcinogenic effects of MCP, the possible proximate metabolite of the alkaloid monocrotaline, were investigated in rats by the subcutaneous route. Sequential of MCP subcutaneously produced an acute inflammatory reaction with necrosis of the local tissue. A slight delay in
Protective effect of beraprost sodium, a stable prostacyclin analogue, in development of monocrotaline-induced pulmonary hypertension.
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Experimental pulmonary hypertension (PH) was induced by a single injection of monocrotaline (MCT), a pyrrolizidine alkaloid extracted from Crotalaria spectabilis. The effect of beraprost sodium, a stable prostacyclin analogue, on the development of MCT-induced PH in rats was studied. Chronic
Anticoagulants prevent monocrotaline-induced hepatic parenchymal cell injury but not endothelial cell injury in the rat.
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Monocrotaline (MCT) is a pyrrolizidine alkaloid plant toxin that produces hepatotoxicity in humans and animals. Human exposure to MCT occurs through consumption of contaminated grains and herbal medicines. Administration of MCT to rats stimulates activation of the coagulation system and fibrin
[Effects of apple polyphenols on monocrotaline-induced pulmonary vascular remodeling in rats and its mechanism].
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METHODS
Rats were randomly divided into 4 groups:control (Con) group, monocrotaline (MCT) group, appleIptakalim ameliorates monocrotaline-induced pulmonary arterial hypertension in rats.
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OBJECTIVE
We sought to investigate the experimental therapeutic effects and mechanisms of iptakalim, a new adenosine triphosphate (ATP)-sensitive potassium channel (K(ATP)) opener, on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) and right heart ventricle remodeling in
Silencing of tissue factor by antisense deoxyoligonucleotide prevents monocrotaline/LPS renal injury in mice.
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Tissue factor (TF) is involved in monocrotaline (MCT)/lipopolysaccharide (LPS) hepatotoxicity. It is not known whether MCT/LPS can cause renal toxicity and whether TF is involved in this toxicity. Thus, the present study was undertaken to investigate the potential renal toxicity after MCT/LPS
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