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| 1 | Consolidated and emerging inflammatory markers in coronary artery disease显示文摘Coronary artery disease is an event of atherosclerosis characterized by a chronic vascular inflammation. Risk factors like obesity, diabetes mellitus, hypertension,smoking, hypercholesterolemia and positive family history sometimes are not sufficiently adequate to the enhancement of cardiovascular risk assessment. In the past years numerous biomarkers, like C reactive protein,cytokines and adhesion molecules, have been observed to be related to adverse cardiovascular prognosis. Recently,several studies found an association among inflammatory biomarkers and cardiovascular diseases suggesting their utility to identify the risk of an acute ischemic event and the detection of vulnerable plaques. The emerginginflammatory markers are well divided for diagnosis and prognosis and plaque instability of coronary artery disease. Some of them, the lectin-like oxidized low density lipoprotein receptor-1 can be important both in diagnosis and in the evaluation of plaque instability, other are inserted in the above reported classification. The emerging inflammatory markers in acute-phase include amyloid A, fibrinogen and pentraxin 3 while myeloperoxidase, myeloid-related protein 8/14 and pregnancy-associated plasma protein-A are recognize markers of plaque instability. Lastly, some studies demonstrated that circulating mi RNAs are involved in coronary artery disease, acute myocardial infarction and heart failure. | Valter Lubrano Silvana Balzan | 2015 | World Journal of Experimental Medicine2015，5，1： | 29 |
| 2 | Lansoprazole prevents experimental gastric injury induced by non-steroidal anti-inflammatory drugs through a reduction of mucosal oxidative damage显示文摘AIM: This study investigated the mechanisms of protection afforded by the proton pump inhibitor lansoprazole against gastric injury induced by different non-steroidal antiinflammatory drugs (NSAIDs) in rats.METHODS: Male Sprague-Dawley rats were orally treated with indomethacin (100 μmol/kg), diclofenac (60 μmol/kg),piroxicam (150 μmol/kg) or ketoprofen (150 μmol/kg).Thirty minutes before NSAIDs, animals were orally treated with lansoprazole 18 or 90 μmol/kg. Four hours after the end of treatments, the following parameters were assessed: gastric mucosal PGE2, malondialdehyde (MDA), myeloperoxidase (MPO) or non-proteic sulfhydryl compounds (GSH) levels; reverse transcription-polymerase chain reaction (RT-PCR) of mucosal COX-2 mRNA; gastric acid secretion in pylorus-ligated animals; in vitro effects of lansoprazole (1-300 μmol/L) on the oxidation of low density lipoproteins (LDLs) induced by copper sulphate.RESULTS: All NSAIDs elicited mucosal necrotic lesions which were associated with neutrophil infiltration and reduction of PGE2 levels. Increments of MPO and MDA contents, as well as a decrease in GSH levels were detected in the gastric mucosa of indomethacin- or piroxicam-treated animals. Indomethacin enhanced mucosal cyclooxygenase-2 expression, while not affecting cyclooxygenase-1. At the oral dose of 18 μmol/kg lansoprazole partly counteracted diclofenac-induced mucosal damage, whereas at 90 μmol/kg it markedly prevented injuries evoked by all test NSAIDs. Lansoprazole at 90 μmol/kg reversed also the effects of NSAIDs on MPO, MDA and GSH mucosal contents, without interfering with the decrease in PGE2 levels or indomethacin-induced cyclooxygenase-2 expression. However, both lansoprazole doses markedly inhibited acid secretion in pylorus-ligated rats. Lansoprazole concentration-dependently reduced the oxidation of LDLs in vitro.CONCLUSION: These results suggest that, besides the inhibition of acid secretion, lansoprazole protection against NSAID-induced gastric damage depends on a reduction in mucosal oxidative injury, which is also responsible for an increment of sulfhydryl radical bioavailability. It is also suggested that lansoprazole does not influence the downregulation of gastric prostaglandin production associated with NSAID treatment. | Corrado Blandizzi Matteo Fornai Rocchina Colucci Gianfranco Natale Valter Lubrano Cristina Vassalle Luca Antonioli Gloria Lazzeri Mario Del Tacca | 2005 | World Journal of Gastroenterology2005，11，26： | 9 |
| 3 | Enzymatic antioxidant system in vascular inflammation and coronary artery disease显示文摘In biological systems there is a balance between the production and neutralization of reactive oxygen species(ROS). This balance is maintained by the presence of natural antioxidants and antioxidant enzymes suchas superoxide dismutase(SOD), catalase and glutathione peroxidase. The enhancement of lipid peroxidation or the decrease of antioxidant protection present in metabolic diseases or bad lifestyle can induce endothelial dysfunction and atherosclerosis.Clinical studies have shown that oxidative stress can increase ROS reducing the formation of antioxidant defences, especially in subjects with coronary artery disease(CAD). Some observation indicated that in the early stages of the disease there is a homeostatic upregulation of the antioxidant enzyme system in response to increased free radicals to prevent vascular damage.As soon as free radicals get to chronically elevated levels, this compensation ceases. Therefore, SOD and the other enzymes may represent a good therapeutic target against ROS, but they are not useful markers for the diagnosis of CAD. In conclusion antioxidant enzymes are reduced in presence of metabolic disease and CAD. However the existence of genes that promote their enzymatic activity could contribute to create new drugs for the treatment of damage caused by metabolic diseases or lifestyle that increases the plasma ROS levels. | Valter Lubrano Silvana Balzan | 2015 | World Journal of Experimental Medicine2015，5，4： | 7 |
| 4 | Proangiogenic Effect of TSH in Human Microvascular Endothelial Cells through Its Membrane Receptor显示文摘 | Silvana Balzan Renata Del Carratore Giuseppina Nicolini Pascale Beffy Valter Lubrano Francesca Forini Giorgio Iervasi | 2012 | The Journal of Clinical Endocrinology & Metabolism2012，，： | 1 |
| 5 | Circulating Levels of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 are Associated with Inflammatory Markers显示文摘 | Valter Lubrano Serena Turco Giuseppina Nicolini Pietro Cecco Giuseppina Basta | 2008 | Lipids2008，，10： | 1 |
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