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Your search keyword '"Ariel R. Marcotegui"' showing total 7 results
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7 results on '"Ariel R. Marcotegui"'

1. AM404, paracetamol metabolite, prevents prostaglandin synthesis in activated microglia by inhibiting COX activity

Author

Soraya Wilke Saliba, Ariel R. Marcotegui, Ellen Fortwängler, Johannes Ditrich, Juan Carlos Perazzo, Eduardo Muñoz, Antônio Carlos Pinheiro de Oliveira, and Bernd L. Fiebich

Subjects
AM404, Acetaminophen, Microglia, Inflammation, Prostaglandins, Cyclooxygenase, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background N-arachidonoylphenolamine (AM404), a paracetamol metabolite, is a potent agonist of the transient receptor potential vanilloid type 1 (TRPV1) and low-affinity ligand of the cannabinoid receptor type 1 (CB1). There is evidence that AM404 exerts its pharmacological effects in immune cells. However, the effect of AM404 on the production of inflammatory mediators of the arachidonic acid pathway in activated microglia is still not fully elucidated. Method In the present study, we investigated the effects of AM404 on the eicosanoid production induced by lipopolysaccharide (LPS) in organotypic hippocampal slices culture (OHSC) and primary microglia cultures using Western blot, immunohistochemistry, and ELISA. Results Our results show that AM404 inhibited LPS-mediated prostaglandin E2 (PGE2) production in OHSC, and LPS-stimulated PGE2 release was totally abolished in OHSC if microglial cells were removed. In primary microglia cultures, AM404 led to a significant dose-dependent decrease in the release of PGE2, independent of TRPV1 or CB1 receptors. Moreover, AM404 also inhibited the production of PGD2 and the formation of reactive oxygen species (8-iso-PGF2 alpha) with a reversible reduction of COX-1- and COX-2 activity. Also, it slightly decreased the levels of LPS-induced COX-2 protein, although no effect was observed on LPS-induced mPGES-1 protein synthesis. Conclusions This study provides new significant insights about the potential anti-inflammatory role of AM404 and new mechanisms of action of paracetamol on the modulation of prostaglandin production by activated microglia.

Published
2017
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2. Correction to: AM404, paracetamol metabolite, prevents prostaglandin synthesis in activated microglia by inhibiting COX activity

Author

Soraya Wilke Saliba, Ariel R. Marcotegui, Ellen Fortwängler, Johannes Ditrich, Juan Carlos Perazzo, Eduardo Muñoz, Antônio Carlos Pinheiro de Oliveira, and Bernd L. Fiebich

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract After publication of the article [1], it has been brought to our attention that the caption for Figure 2 has been mistakenly replaced with a reproduction of the Figure 4 caption.

Published
2018
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3. Menhaden oil rich diet and experimental renal damage due to ischemia reperfusion

Author

Ana Uceda, Georgina P. Ossani, Juan Carlos Perazzo, Néstor Lago, Alberto J. Monserrat, and Ariel R. Marcotegui

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, General Chemical Engineering, ISCHEMIA REPERFUSION, Inmunología, Ischemia, ACUTE KIDNEY INJURY, MENHADEN OIL, Gastroenterology, 03 medical and health sciences, Fish Oils, 0302 clinical medicine, Internal medicine, medicine, Animals, HISTOPATHOLOGICAL DAMAGE, Rats, Wistar, Menhaden Oil, 030109 nutrition & dietetics, Renal damage, business.industry, Acute kidney injury, 030208 emergency & critical care medicine, General Medicine, General Chemistry, purl.org/becyt/ford/3.1 [https], Acute Kidney Injury, medicine.disease, Disease Models, Animal, Medicina Básica, Reperfusion Injury, Dietary Supplements, purl.org/becyt/ford/3 [https], business
Abstract

Renal necrosis can be induced in weanling rats due to choline deficient diet. Menhaden oil has a protective effect against the development of renal necrosis in choline deficient weanling rats. The aim of this work was to determine the effects of menhaden oil in a model of acute kidney injury due to ischemia reperfusion. Wistar rats were divided into two groups and fed vegetable oils or menhaden oil as lipids. Unilateral renal ischemia was performed for 30 minutes and animals were sacrificed 48 hours later. Histopathological examination showed no significant differences between groups. Menhaden oil did not prevent histopathological lesions. Fil: Ossani, Georgina Paula. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina Fil: Marcotegui, Ariel R.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina Fil: Uceda, Ana Margarita. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina Fil: Monserrat, Alberto Juan. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina Fil: Lago, Néstor Rubén. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina Fil: Perazzo, Juan C.. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina

Published
2017

5. Correction to: AM404, paracetamol metabolite, prevents prostaglandin synthesis in activated microglia by inhibiting COX activity

Author

Ellen Fortwängler, Soraya Wilke Saliba, Johannes Ditrich, Juan Carlos Perazzo, Antônio Carlos Pinheiro de Oliveira, Ariel R. Marcotegui, Eduardo Muñoz, and Bernd L. Fiebich

Subjects
0301 basic medicine, Metabolite, Immunology, Anti-Inflammatory Agents, Arachidonic Acids, Pharmacology, lcsh:RC346-429, Rats, Sprague-Dawley, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, 0302 clinical medicine, Animals, Medicine, Cyclooxygenase Inhibitors, Cells, Cultured, lcsh:Neurology. Diseases of the nervous system, Acetaminophen, Microglia, business.industry, General Neuroscience, Prostaglandin synthesis, Correction, Rats, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, Neurology, chemistry, Cyclooxygenase 2, AM404, Cyclooxygenase 1, Prostaglandins, business, 030217 neurology & neurosurgery
Abstract

N-arachidonoylphenolamine (AM404), a paracetamol metabolite, is a potent agonist of the transient receptor potential vanilloid type 1 (TRPV1) and low-affinity ligand of the cannabinoid receptor type 1 (CB1). There is evidence that AM404 exerts its pharmacological effects in immune cells. However, the effect of AM404 on the production of inflammatory mediators of the arachidonic acid pathway in activated microglia is still not fully elucidated.In the present study, we investigated the effects of AM404 on the eicosanoid production induced by lipopolysaccharide (LPS) in organotypic hippocampal slices culture (OHSC) and primary microglia cultures using Western blot, immunohistochemistry, and ELISA.Our results show that AM404 inhibited LPS-mediated prostaglandin EThis study provides new significant insights about the potential anti-inflammatory role of AM404 and new mechanisms of action of paracetamol on the modulation of prostaglandin production by activated microglia.

Published
2018

6. Hepatic encephalopathy: Ever closer to its big bang

Author

Juan Skerl, Juan Carlos Perazzo, Ariel R. Marcotegui, Pablo A. Souto, and Lisandro Orbea

Subjects
medicine.medical_specialty, Cirrhosis, Minimal hepatic encephalopathy, Skeletal muscle, Physiology, Biology, Pathogenesis, 03 medical and health sciences, Liver disease, 0302 clinical medicine, Ammonia, Internal medicine, Small intestinal bacterial overgrowth, medicine, Animals, Humans, Hyperammonemia, Intestinal Mucosa, Muscle, Skeletal, Hepatic encephalopathy, Gastroenterology, General Medicine, Prognosis, medicine.disease, Intestines, Glutamine, Editorial, Endocrinology, medicine.anatomical_structure, Liver, Hepatic Encephalopathy, Disease Progression, 030211 gastroenterology & hepatology, 030217 neurology & neurosurgery
Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that commonly complicates the course of patients with liver disease. Despite the fact that the syndrome was probably first recognized hundreds of years ago, the exact pathogenesis still remains unclear. Minimal hepatic encephalopathy (MHE) is the earliest form of HE and is estimated to affect more that 75% of patients with liver cirrhosis. It is characterized by cognitive impairment predominantly attention, reactiveness and integrative function with very subtle clinical manifestations. The development of MHE is associated with worsen in driving skills, daily activities and the increase of overall mortality. Skeletal muscle has the ability to shift from ammonia producer to ammonia detoxifying organ. Due to its large size, becomes the main ammonia detoxifying organ in case of chronic liver failure and muscular glutamine-synthase becomes important due to the failing liver and brain metabolic activity. Gut is the major glutamine consumer and ammonia producer organ in the body. Hepatocellular dysfunction due to liver disease, results in an impaired clearance of ammonium and in its inter-organ trafficking. Intestinal bacteria, can also represent an extra source of ammonia production and in cirrhosis, small intestinal bacterial overgrowth and symbiosis can be observed. In the study of HE, to get close to MHE is to get closer to its big bang; and from here, to travel less transited roads such as skeletal muscle and intestine, is to go even closer. The aim of this editorial is to expose this road for further and deeper work.

Published
2016

7. Hepatic encephalopathy: Ever closer to its big bang.

Author

Souto PA, Marcotegui AR, Orbea L, Skerl J, and Perazzo JC

Subjects
Animals, Disease Progression, Hepatic Encephalopathy complications, Hepatic Encephalopathy pathology, Humans, Intestines ultrastructure, Liver ultrastructure, Muscle, Skeletal ultrastructure, Prognosis, Ammonia metabolism, Hepatic Encephalopathy metabolism, Intestinal Mucosa metabolism, Liver metabolism, Muscle, Skeletal metabolism
Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that commonly complicates the course of patients with liver disease. Despite the fact that the syndrome was probably first recognized hundreds of years ago, the exact pathogenesis still remains unclear. Minimal hepatic encephalopathy (MHE) is the earliest form of HE and is estimated to affect more that 75% of patients with liver cirrhosis. It is characterized by cognitive impairment predominantly attention, reactiveness and integrative function with very subtle clinical manifestations. The development of MHE is associated with worsen in driving skills, daily activities and the increase of overall mortality. Skeletal muscle has the ability to shift from ammonia producer to ammonia detoxifying organ. Due to its large size, becomes the main ammonia detoxifying organ in case of chronic liver failure and muscular glutamine-synthase becomes important due to the failing liver and brain metabolic activity. Gut is the major glutamine consumer and ammonia producer organ in the body. Hepatocellular dysfunction due to liver disease, results in an impaired clearance of ammonium and in its inter-organ trafficking. Intestinal bacteria, can also represent an extra source of ammonia production and in cirrhosis, small intestinal bacterial overgrowth and symbiosis can be observed. In the study of HE, to get close to MHE is to get closer to its big bang; and from here, to travel less transited roads such as skeletal muscle and intestine, is to go even closer. The aim of this editorial is to expose this road for further and deeper work., Competing Interests: Conflict-of-interest statement: The authors declare that they don´t have any conflict of interest.

Published
2016
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