EZQUER, EDUARDO FERNANDO
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EZQUER, EDUARDO FERNANDO
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eezquer@udd.cl
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8614146900

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Morphine self-administration is inhibited by the antioxidant N‐acetylcysteine and the anti-inflammatory ibudilast; an effect enhanced by their co-administration

2024 , María Elena Quintanilla , Paola Morales , Daniela Santapau , Javiera Gallardo , Rocío Rebolledo , Gabriel Riveras , Tirso Acuña , Mario Herrera-Marschitz , Yedy Israel , EZQUER, EDUARDO FERNANDO , Shao-Jun Tang

Background The treatment of opioid addiction mainly involves the medical administration of methadone or other opioids, aimed at gradually reducing dependence and, consequently, the need for illicit opioid procurement. Thus, initiating opioid maintenance therapy with a lower level of dependence would be advantageous. There is compelling evidence indicating that opioids induce brain oxidative stress and associated glial activation, resulting in the dysregulation of glutamatergic homeostasis, which perpetuates drug intake. The present study aimed to determine whether inhibiting oxidative stress and/or neuroinflammation reduces morphine self-administration in an animal model of opioid dependence. Methods Morphine dependence, assessed as voluntary morphine self-administration, was evaluated in Wistar-derived UChB rats. Following an extended period of morphine self-administration, animals were administered either the antioxidant N-acetylcysteine (NAC; 40 mg/kg/day), the anti-inflammatory ibudilast (7.5 mg/kg/day) or the combination of both agents. Oxidative stress and neuroinflammation were evaluated in the hippocampus, a region involved in drug recall that feeds into the nucleus accumbens, where the levels of the glutamate transporters GLT-1 and xCT were further assessed. Results Daily administration of either NAC or ibudilast led to a mild reduction in voluntary morphine intake, while the co-administration of both therapeutic agents resulted in a marked inhibition (-57%) of morphine self-administration. The administration of NAC or ibudilast markedly reduced both the oxidative stress induced by chronic morphine intake and the activation of microglia and astrocytes in the hippocampus. However, only the combined administration of NAC + ibudilast was able to restore the normal levels of the glutamate transporter GLT-1 in the nucleus accumbens. Conclusion Separate or joint administration of an antioxidant and anti-inflammatory agent reduced voluntary opioid intake, which could have translational value for the treatment of opioid use disorders, particularly in settings where the continued maintenance of oral opioids is a therapeutic option.

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Corrigendum: Contribution of Connexin Hemichannels to the Decreases in Cell Viability Induced by Linoleic Acid in the Human Lens Epithelial Cells (HLE-B3)

2020 , Vania A. Figueroa , Oscar Jara , Carolina A. Oliva , EZQUER, EDUARDO MARCELO , EZQUER, EDUARDO FERNANDO , RETAMAL LUCERO, MAURICIO ANTONIO , Agustín D. Martínez , Guillermo A. Altenberg , Aníbal A. Vargas

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Tubulointerstitial injury and proximal tubule albumin transport in early diabetic nephropathy induced by type 1 diabetes mellitus

2018 , M. Giraud Billoud , EZQUER, EDUARDO FERNANDO , J. Bahamonde , EZQUER, EDUARDO MARCELO

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Chronic Voluntary Morphine Intake Is Associated with Changes in Brain Structures Involved in Drug Dependence in a Rat Model of Polydrug Use

2023 , María Elena Quintanilla , Paola Morales , Daniela Santapau , Alba Ávila , Carolina Ponce , BERRIOS CARCAMO, PABLO ANDRES , OLIVARES, MARIA BELEN , Mario Herrera-Marschitz , EZQUER, EDUARDO MARCELO , Javiera Gallardo , Yedy Israel , EZQUER, EDUARDO FERNANDO

Chronic opioid intake leads to several brain changes involved in the development of dependence, whereby an early hedonistic effect (liking) extends to the need to self-administer the drug (wanting), the latter being mostly a prefrontal–striatal function. The development of animal models for voluntary oral opioid intake represents an important tool for identifying the cellular and molecular alterations induced by chronic opioid use. Studies mainly in humans have shown that polydrug use and drug dependence are shared across various substances. We hypothesize that an animal bred for its alcohol preference would develop opioid dependence and further that this would be associated with the overt cortical abnormalities clinically described for opioid addicts. We show that Wistar-derived outbred UChB rats selected for their high alcohol preference additionally develop: (i) a preference for oral ingestion of morphine over water, resulting in morphine intake of 15 mg/kg/day; (ii) marked opioid dependence, as evidenced by the generation of strong withdrawal signs upon naloxone administration; (iii) prefrontal cortex alterations known to be associated with the loss of control over drug intake, namely, demyelination, axonal degeneration, and a reduction in glutamate transporter GLT-1 levels; and (iv) glial striatal neuroinflammation and brain oxidative stress, as previously reported for chronic alcohol and chronic nicotine use. These findings underline the relevance of polydrug animal models and their potential in the study of the wide spectrum of brain alterations induced by chronic morphine intake. This study should be valuable for future evaluations of therapeutic approaches for this devastating condition.

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Intragastric administration of short chain fatty acids greatly reduces voluntary ethanol intake in rats

2024 , María Elena Quintanilla , Daniela Santapau , Eugenio Diaz , Ignacio Valenzuela Martinez , Nicolas Medina , Glauben Landskron , Antonia Dominguez , Paola Morales , David Ramírez , Marcela Hermoso , Belén Olivares , Pablo Berríos-Cárcamo , EZQUER, EDUARDO MARCELO , Mario Herrera-Marschitz , Yedy Israel , EZQUER, EDUARDO FERNANDO

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Preconditioning of adipose tissue-derived mesenchymal stem cells with deferoxamine increases the production of pro-angiogenic, neuroprotective and anti-inflammatory factors: Potential application in the treatment of diabetic neuropathy

2017 , Carolina Oses , OLIVARES, MARIA BELEN , EZQUER, EDUARDO MARCELO , Cristian Acosta , BOSCH PÉREZ, PAUL JESÚS , Macarena Donoso , Patricio Léniz , EZQUER, EDUARDO FERNANDO

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Contribution of connexin hemichannels to the decreases in cell viability induced by linoleic acid in the human lens epithelial cells (HLE-B3)

2020 , Vania A. Figueroa , Oscar Jara , Carolina A. Oliva , EZQUER, EDUARDO MARCELO , EZQUER, EDUARDO FERNANDO , RETAMAL LUCERO, MAURICIO ANTONIO , Agustín D. Martínez , Guillermo A. Altenberg , Aníbal A. Vargas

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Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice

2024 , BERRIOS CARCAMO, PABLO ANDRES , Sarah Núñez , Justine Castañeda , GALLARDO ROJAS, JAVERA CAROLINA , María Rosa Bono , EZQUER, EDUARDO FERNANDO

Chronic ethanol exposure often triggers neuroinflammation in the brain’s reward system, potentially promoting the drive for ethanol consumption. A main marker of neuroinflammation is the microglia-derived monocyte chemoattractant protein 1 (MCP1) in animal models of alcohol use disorder in which ethanol is forcefully given. However, there are conflicting findings on whether MCP1 is elevated when ethanol is taken voluntarily, which challenges its key role in promoting motivation for ethanol consumption. Here, we studied MCP1 mRNA levels in areas implicated in consumption motivation—specifically, the prefrontal cortex, hippocampus, and striatum—as well as in the cerebellum, a brain area highly sensitive to ethanol, of C57BL/6 mice subjected to intermittent and voluntary ethanol consumption for two months. We found a significant increase in MCP1 mRNA levels in the cerebellum of mice that consumed ethanol compared to controls, whereas no significant changes were observed in the prefrontal cortex, hippocampus, or striatum or in microglia isolated from the hippocampus and striatum. To further characterize cerebellar neuroinflammation, we measured the expression changes in other proinflammatory markers and chemokines, revealing a significant increase in the proinflammatory microRNA miR-155. Notably, other classical proinflammatory markers, such as TNFα, IL6, and IL-1β, remained unaltered, suggesting mild neuroinflammation. These results suggest that the onset of neuroinflammation in motivation-related areas is not required for high voluntary consumption in C57BL/6 mice. In addition, cerebellar susceptibility to neuroinflammation may be a trigger to the cerebellar degeneration that occurs after chronic ethanol consumption in humans.

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Aspirin and N‐acetylcysteine co‐administration markedly inhibit chronic ethanol intake and block relapse binge drinking: Role of neuroinflammation‐oxidative stress self‐perpetuation

2019 , Yedy Israel , María Elena Quintanilla , EZQUER, EDUARDO FERNANDO , Paola Morales , Daniela Santapau , BERRIOS CARCAMO, PABLO ANDRES , EZQUER, EDUARDO MARCELO , OLIVARES, MARIA BELEN , Mario Herrera‐Marschitz

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IMMUNOMODULATORY AND REGENERATIVE PROPERTIES OF HUMAN MENSENCHYMAL STEM CELLS SECRETOME, PREVENT HEPATIC AND RENAL MULTIPLE ORGAN DYSFUNCTION IN A RAT MODEL OF ACUTE ON CHRONIC LIVER FAILURE

2023 , EZQUER, EDUARDO FERNANDO , EZQUER, EDUARDO MARCELO

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