Publications by authors named "Maria Bove"

19 Publications

  • Page 1 of 1

Sublingual AKBA Exerts Antidepressant Effects in the Aβ-Treated Mouse Model.

Biomolecules 2021 May 3;11(5). Epub 2021 May 3.

Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.

The 3-O-acetyl-11-keto-β-boswellic acid (AKBA) is the most active compound of proposed for treating neurodegenerative disorders, including Alzheimer's disease (AD), characterized in its early phase by alteration in mood. Accordingly, we have previously demonstrated that an intracerebroventricular injection of soluble amyloid beta (Aβ) peptide evokes a depressive-like phenotype in rats. We tested the protective effects of AKBA in the mouse model of an Aβ-induced depressive-like phenotype. We evaluated the depressive-like behavior by using the tail suspension test (TST) and the splash test (ST). Behavioral analyses were accompanied by neurochemical quantifications, such as glutamate (GLU), kynurenine (KYN) and monoamines, and by biochemical measurements, such as glial fibrillary acid protein (GFAP), CD11b and nuclear factor kappa B (NF-kB), in mice prefrontal cortex (PFC) and hippocampus (HIPP). AKBA prevented the depressive-like behaviors induced by Aβ administration, since we recorded a reduction in latency to initiate self-care and total time spent to perform self-care in the ST and reduced time of immobility in the TST. Likewise, the increase in GLU and KYN levels in PFC and HIPP induced by the peptide injection were reverted by AKBA administration, as well as the displayed increase in levels of GFAP and NF-kB in both PFC and HIPP, but not in CD11b. Therefore, AKBA might represent a food supplement suitable as an adjuvant for therapy of depression in early-stage AD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/biom11050686DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8170916PMC
May 2021

N-3 PUFA Prevent Oxidative Stress in a Rat Model of Beta-Amyloid-Induced Toxicity.

Pharmaceuticals (Basel) 2021 Apr 8;14(4). Epub 2021 Apr 8.

Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.

Polyunsaturated fatty acids (PUFA) are involved in brain disorders associated to amyloid beta (Aβ) toxicity for which oxidative stress, neurochemical dysfunctions, and neuroinflammation are underlying mechanisms. Here, mechanisms through which lifelong exposure to n-3 PUFA-enriched or n-6/n-3 balanced diets could elicit a protective role in a rat model of Aβ-induced toxicity were investigated. To this aim, we quantified hippocampal reactive oxygen species (ROS) amount, 8-hydroxy-2'-deoxyguanosine and interleukin-10 levels, NADPH oxidase (NOX) 1, NOX2, superoxide dismutase 1, and glutathione contents, as well as plasmatic malondialdehyde. Moreover, in the same experimental groups, we assessed tryptophan, serotonin, and its turnover, kynurenine, and noradrenaline amounts. Results showed increased hippocampal ROS and NOX2 levels, serotonin turnover, kynurenine, and noradrenaline contents in Aβ-treated rats. Both n-6/n-3 balanced and n-3 PUFA enriched diets reduced ROS production, NOX1 and malondialdehyde levels, serotonin turnover, and kynurenine amount in Aβ-injected rats, while increasing NOX2, superoxide dismutase 1, and serotonin contents. No differences in plasmatic coenzyme Q10, reduced glutathione (GSH) and tryptophan levels were detected among different experimental groups, whereas GSH + oxidized glutathione (GSSG) levels were increased in sham animals fed with n-3 PUFA enriched diet and in Aβ-treated rats exposed to both n-6/n-3 balanced and n-3 enriched diets. In addition, Aβ-induced decrease of interleukin-10 levels was prevented by n-6/n-3 PUFA balanced diet. N-3 PUFA enriched diet further increased interleukin-10 and 8-hydroxy-2'-deoxyguanosine levels. In conclusion, our data highlight the possible neuroprotective role of n-3 PUFA in perturbation of oxidative equilibrium induced by Aβ-administration.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ph14040339DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8068120PMC
April 2021

NT3/TrkC Pathway Modulates the Expression of UCP-1 and Adipocyte Size in Human and Rodent Adipose Tissue.

Front Endocrinol (Lausanne) 2021 18;12:630097. Epub 2021 Mar 18.

Departamento de Farmacología, Facultad de Farmacia, Universidad de Valencia, Valencia, Spain.

(NT3), through activation of its tropomyosin-related kinase receptor C (TrkC), modulates neuronal survival and neural stem cell differentiation. It is widely distributed in peripheral tissues (especially vessels and pancreas) and this ubiquitous pattern suggests a role for NT3, outside the nervous system and related to metabolic functions. The presence of the NT3/TrkC pathway in the adipose tissue (AT) has never been investigated. Present work studies in human and murine adipose tissue (AT) the presence of elements of the NT3/TrkC pathway and its role on lipolysis and adipocyte differentiation. qRT-PCR and immunoblot indicate that NT3 (encoded by ) was present in human retroperitoneal AT and decreases with age. NT3 was also present in rat isolated adipocytes and retroperitoneal, interscapular, perivascular, and perirenal AT. Histological analysis evidences that NT3 was mainly present in vessels irrigating AT close associated to sympathetic fibers. Similar mRNA levels of TrkC (encoded by ) and β-adrenoceptors were found in all ATs assayed and in isolated adipocytes. NT3, through TrkC activation, exert a mild effect in lipolysis. Addition of NT3 during the differentiation process of human pre-adipocytes resulted in smaller adipocytes and increased uncoupling protein-1 (UCP-1) without changes in β-adrenoceptors. Similarly, transgenic mice with reduced expression of NT3 (Ntf3 knock-in lacZ reporter mice) or lacking endothelial NT3 expression (Ntf3flox1/flox2;Tie2-Cre+/0) displayed enlarged white and brown adipocytes and lower UCP-1 expression.

Conclusions: NT3, mainly released by blood vessels, activates TrkC and regulates adipocyte differentiation and browning. Disruption of NT3/TrkC signaling conducts to hypertrophied white and brown adipocytes with reduced expression of the thermogenesis marker UCP-1.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fendo.2021.630097DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8015941PMC
March 2021

Postnatal Antioxidant and Anti-inflammatory Treatments Prevent Early Ketamine-Induced Cortical Dysfunctions in Adult Mice.

Front Neurosci 2020 4;14:590088. Epub 2020 Nov 4.

Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.

Early brain insult, interfering with its maturation, may result in psychotic-like disturbances in adult life. Redox dysfunctions and neuroinflammation contribute to long-term psychiatric consequences due to neurodevelopmental abnormalities. Here, we investigated the effects of early pharmacological modulation of the redox and inflammatory states, through celastrol, and indomethacin administration, on reactive oxygen species (ROS) amount, levels of malondialdehyde (MDA) and antioxidant enzymes (superoxide dismutase 1, SOD1, glutathione, GSH, and catalase, CAT), as well as of pro-inflammatory cytokines (tumor necrosis factor-alpha, TNF-α, interleukin-6, IL-6, and interleukin-1 beta, IL-1β), in the prefrontal cortex of adult mice exposed to a neurotoxic insult, i.e. ketamine administration, in postnatal life. Early celastrol or indomethacin prevented ketamine-induced elevations in cortical ROS production. MDA levels in ketamine-treated mice, also administered with celastrol, were comparable with the control ones. Indomethacin also prevented the increase in lipid peroxidation following early ketamine administration. Whereas no significant differences were detected in SOD1, GSH, and CAT levels between ketamine and saline-administered mice, celastrol elevated the cortical amount of these antioxidant enzymes and the same effect was induced by indomethacin . Both celastrol and indomethacin prevented ketamine-induced enhancement in TNF-α and IL-1β levels, however, they had no effects on increased IL-6 amount resulting from ketamine exposure in postnatal life. In conclusion, our data suggest that an early increase in cortical ROS scavenging and reduction of lipid peroxidation, via the enhancement of antioxidant defense, together with inhibition of neuroinflammation, may represent a therapeutic opportunity against psychotic-like disturbances resulting, later in life, from the effects of a neurotoxic insult on the developing brain.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fnins.2020.590088DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7672215PMC
November 2020

Ketamine administration induces early and persistent neurochemical imbalance and altered NADPH oxidase in mice.

Prog Neuropsychopharmacol Biol Psychiatry 2020 01 22;96:109750. Epub 2019 Aug 22.

Department of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, Piazzale Aldo Moro, 5, 00185 Rome, Italy. Electronic address:

Administration in adulthood of subanaesthetic doses of ketamine, an NMDA receptor (NMDA-R) antagonist, is commonly used to induce psychotic-like alterations in rodents. The NADPH oxidase (NOX) derived-oxidative stress has been shown to be implicated in ketamine-induced neurochemical dysfunctions and in the loss of parvalbumin (PV)-positive interneurons associated to the administration of this NMDA receptor antagonist in adult mice. However, very few data are available on the effects of early ketamine administration and its contribution to the development of long-term dysfunctions leading to psychosis. Here, by administering a subanaesthetic dose of ketamine (30 mg/kg i.p.) to mice at postnatal days (PNDs) 7, 9 and 11, we aimed at investigating early neurochemical and oxidative stress-related alterations induced by this NMDA-R antagonist in specific brain regions of mice pups, i.e. prefrontal cortex (PFC) and nucleus accumbens (NAcc) and to assess whether these alterations lasted until the adult period. To this purpose, we evaluated glutamatergic, glutamine and GABAergic tissue levels, as well as PV amount in the PFC, both two hours after the last ketamine injection (PND 11) and at 10  weeks of age. Dopamine (DA) tissue levels and DA turnover were also evaluated in the NAcc at the same time points. Levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a reliable biomarker of oxidative stress, as well as of the free radical producers NOX1 and NOX2 enzymes, were also assessed in both PFC and NAcc of ketamine-treated pups and adult mice. Ketamine-treated pups showed increased cortical levels of glutamate (GLU) and glutamine, as well as similar GABA amount compared to controls, together with an early reduction of cortical PV levels. In the adult period, the same was observed for GLU and PV, whereas GABA levels were increased and no changes in glutamine amount were detected. Ketamine administration in early life induced a decrease in DA tissue levels and an increase of DA turnover which were also detectable at 10 weeks of age. These alterations were accompanied by 8-OHdG elevations in both PFC and NAcc at the two considered life stages. The expression of NOX1 was significantly reduced in these brain regions following ketamine administration at early life stages, while, in the adult period, significant elevation of this enzyme was observed. Levels of NOX2 were found increased at both time points. Our results suggest that an early increase of NOX2-derived oxidative stress may contribute to the development of neurochemical imbalance in PFC and NAcc, induced by ketamine administration. Modifications of NOX1 expression might represent, instead, an early response of the developing brain to a neurotoxic insult, followed by a later attempt to counterbalance ketamine-related detrimental effects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.pnpbp.2019.109750DOI Listing
January 2020

A long-term treatment with taurine prevents cardiac dysfunction in mdx mice.

Transl Res 2019 02 28;204:82-99. Epub 2018 Sep 28.

Section of Pharmacology, Department of Pharmacy - Drug Sciences, University of Bari "A. Moro", Bari, Italy. Electronic address:

Taurine is an amino acid abundantly present in heart and skeletal muscle. Duchenne muscular dystrophy (DMD) is a genetic disorder in which the absence of dystrophin leads to skeletal muscle wasting and heart failure. An altered taurine metabolism has been described in dystrophic animals and short-term taurine administration exerts promising amelioration of early muscular alterations in the mdx mouse model of DMD. To reinforce the therapeutic and nutraceutical taurine potential in DMD, we evaluated the effects of a long-term treatment on cardiac and skeletal muscle function of mdx mice in a later disease stage. Taurine was administered in drinking water (1 g/kg/day) to wt and mdx mice for 6 months, starting at 6 months of age. Ultrasonography evaluation of heart and hind limb was performed, in parallel with in vivo and ex vivo functional tests and biochemical, histological and gene expression analyses. 12-month-old mdx mice showed a significant worsening of left ventricular function parameters (shortening fraction, ejection fraction, stroke volume), which were significantly counteracted by the taurine treatment. In parallel, histologic signs of damage were reduced by taurine along with the expression of proinflammatory myocardial IL-6. Interestingly, no effects were observed on hind limb volume and percentage of vascularization or on in vivo and ex vivo muscle functional parameters, suggesting a tissue-specific action of taurine in relation to the disease phase. A trend toward increase in taurine was found in heart and quadriceps from treated animals, paralleled by a slight decrease in mdx mice plasma. Our study provides evidences that taurine can prevent late heart dysfunction in mdx mice, further corroborating the interest on this amino acid toward clinical trials.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.trsl.2018.09.004DOI Listing
February 2019

Effects of n-3 PUFA enriched and n-3 PUFA deficient diets in naïve and Aβ-treated female rats.

Biochem Pharmacol 2018 09 17;155:326-335. Epub 2018 Jul 17.

Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy. Electronic address:

Depression is one of the most common psychiatric diseases and the prevalence of depressive symptoms in women is almost twice compared to men, although the reasons of this gender difference are not fully understood yet. Recently, soluble Aβ peptide has been receiving great importance in the development of depression, also since depression is highly comorbid with Alzheimer's disease and other neurodegenerative illnesses. Accordingly, we have previously shown that central Aβ injection is able to elicit depressive-like phenotype in male rats. In the present study, we reproduced for the first time the Aβ-induced depressive-like model in female rats, evaluating behavioural and neurochemical outcomes. Moreover, we studied the effect of lifelong exposure to either n-3 PUFA enriched or n-3 PUFA deficient diet, in female rats, both intact and after central Aβ administration. Our results confirmed the Aβ-induced depressive-like profile also in female rats. Moreover, chronic exposure to n-3 PUFA deficient diet led to highly negative alterations in behavioural and neurochemical parameters, while lifelong exposure to n-3 PUFA enriched diet was able to restore the Aβ-induced depressive-like profile in female rats. In conclusion, the Aβ-induced depressive-like profile was reversed by n-3 PUFA supplementation, indicating a possible therapeutic role of n-3 PUFA in the treatment of the burden of depressive disorders.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bcp.2018.07.017DOI Listing
September 2018

Design and Objectives of the South American Youth/Child Cardiovascular and Environmental (SAYCARE) Study.

Obesity (Silver Spring) 2018 03;26 Suppl 1:S5-S13

Youth/Child Cardiovascular Risk and Environmental Research Group, Department of Preventive Medicine, School of Medicine, University of São Paulo, São Paulo, São Paulo, Brazil.

Objective: The purpose of this paper is to introduce the overarching study design of the South American Youth/Child Cardiovascular and Environmental (SAYCARE) study, which is an observational multicenter feasibility study held in seven South American cities: Buenos Aires (Argentina), Lima (Peru), Medellin (Colombia), Montevideo (Uruguay), Santiago (Chile), and São Paulo and Teresina (Brazil). Children and adolescents (3-17 years of age) were studied.

Methods: The data management systems, quality assurance monitoring activities, standardized operating procedure manuals, and training and study management are addressed in this paper. Various quality controls to ensure the collection of valid and reliable data are also discussed.

Results And Conclusions: Data were obtained from 237 preschoolers and schoolchildren and 258 adolescents during the validation phase measurements. The results of the SAYCARE study are expected to provide higher accuracy in the assessment of cardiovascular disease risk factors, including eating behaviors, body composition, physical activity, sedentary behaviors, lipid profiles and cardiovascular health biomarkers, oral health, social conditions, environmental factors and home environment, and their determinants in children and adolescents from ages 3 to 17 in seven South American cities.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/oby.22117DOI Listing
March 2018

The Visible Burrow System: A behavioral paradigm to assess sociability and social withdrawal in BTBR and C57BL/6J mice strains.

Behav Brain Res 2018 05 7;344:9-19. Epub 2018 Feb 7.

Groningen Institute for Evolutionary Life Science, University of Groningen, Nijenborgh 7, 9747 AG, Groningen, The Netherlands. Electronic address:

Disrupted sociability and consequent social withdrawal are (early) symptoms of a wide variety of neuropsychiatric diseases, such as schizophrenia, autism spectrum disorders, depressive disorders and Alzheimer's disease. The paucity of objective measures to translationally assess social withdrawal characteristics has been an important limitation to study this behavioral phenotype, both in human and rodents. The aim of the present study was to investigate sociability and social withdrawal in rodents using an ethologically valid behavioral paradigm, the Visible Burrow System (VBS). The VBS mimics a natural environment, with male and female rodents housed together in an enclosure where a large open arena is connected to a continuously dark burrow system that includes 4 nest boxes. In this study, mixed-sex colonies of C57BL/6J and of BTBR mice have been investigated (n = 8 mice per colony). Results showed marked differences between the two strains, in terms of sociability as well as social withdrawal behaviors. In particular, BTBR mice performed less social behaviors and have a preference for non-social behaviors compared to C57BL/6J mice. Neurobiologically, the decreased sociability of BTBR was accompanied by reduced GABA and increased glutamate concentrations in brain prefrontal cortex (PFC) and amygdala regions. In conclusion, our study validated the use of the VBS as an ethologically relevant behavioral paradigm in group-housed mice to investigate individual sociability and social withdrawal features and their underlying neurobiology. This paradigm may provide new insights to develop new therapeutic treatments for behavioral dysfunctions that may be relevant across neuropsychiatric diseases.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbr.2018.02.003DOI Listing
May 2018

Celecoxib Prevents Cognitive Impairment and Neuroinflammation in Soluble Amyloid β-treated Rats.

Neuroscience 2018 02 3;372:58-73. Epub 2018 Jan 3.

Dept. of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy. Electronic address:

Recent findings suggest that soluble forms of amyloid-β (sAβ) peptide contribute to synaptic and cognitive dysfunctions in early stages of Alzheimer's disease (AD). On the other hand, neuroinflammation and cyclooxygenase-2 (COX-2) enzyme have gained increased interest as key factors involved early in AD, although the signaling pathways and pathophysiologic mechanisms underlying a link between sAβ-induced neurotoxicity and inflammation are still unclear. Here, we investigated the effects of selective COX-2 enzyme inhibition on neuropathological alterations induced by sAβ administration in rats. To this purpose, animals received an intracerebroventricular (icv) injection of predominantly monomeric forms of sAβ and, 7 days after, behavioral as well as biochemical parameters and neurotransmitter alterations were evaluated. During this period, rats also received a sub-chronic treatment with celecoxib. Biochemical results demonstrated that icv sAβ injection significantly increased both COX-2 and pro-inflammatory cytokines expression in the hippocampus (Hipp) of treated rats. In addition, the number of hypertrophic microglial cells and astrocytes were upregulated in sAβ-treated group. Interestingly, rats treated with sAβ showed long-term memory deficits, as confirmed by a significant reduction of discrimination index in the novel object recognition test, along with reduced brain-derived neurotrophic factor expression and increased noradrenaline levels in the Hipp. Systemic administration of celecoxib prevented behavioral dysfunctions, as well as biochemical and neurotransmitter alterations. In conclusion, our results suggest that sAβ neurotoxicity might be associated to COX-2-mediated inflammatory pathways and that early treatment with selective COX-2 inhibitor might provide potential remedies to counterbalance the sAβ-induced effects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.neuroscience.2017.12.046DOI Listing
February 2018

Visceral Fat Dysfunctions in the Rat Social Isolation Model of Psychosis.

Front Pharmacol 2017 8;8:787. Epub 2017 Nov 8.

Department of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.

Medication with neuroleptics has been associated with adipose tissue dysfunctions and, in particular, with increased visceral fat amount. However, several studies suggested that antipsychotic treatment might not be the main responsible of fat mass accumulation, as this has been also described in not treated psychotic patients. One of the most used "drug-free" rodent models of psychosis is the social isolation rearing of young adult rats, which provides a non-pharmacologic method of inducing long-term alterations reminiscent of symptoms seen in psychotic patients. Recent data highlighted a crucial role of redox imbalance in adipose tissue dysfunctions, in terms of decreased antioxidant defense and increased reactive oxygen species (ROS). Here, we investigated possible oxidative stress-related biomolecular alterations associated with visceral fat increase in 7 week isolated rats. To this purpose, we quantified total and visceral fat amount by using dual-energy X-ray (DEXA) absorptiometry. On visceral fat, we analyzed the expression of specific ROS-producer genes (), antioxidant enzymes ( and ) and oxidative stress-induced damage markers (, and ). The impact of oxidative stress on beta3-adrenergic receptors (), at both mRNA and protein level, was also assessed. We found that 7 weeks of social isolation induced an increase in total and visceral fat, associated with a decrease in (mRNA and protein) as well as mRNA levels and an enhanced expression of (mRNA and protein) and mRNA. No differences were detected in mRNA levels between grouped and isolated animals. Elevations in , , and expression in visceral fat of isolated animals accounted for oxidative stress-related damage in this tissue, further associated with a significant increase in mRNA and protein. Our results provide a novel understanding of the pathological link existing among psychosocial stress-induced psychosis, adipose tissue dysfunctions and redox imbalance, opening new therapeutic perspectives for the treatment of alterations in peripheral tissues associated with this mental disorder.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2017.00787DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5682313PMC
November 2017

Antidepressant drugs for beta amyloid-induced depression: A new standpoint?

Prog Neuropsychopharmacol Biol Psychiatry 2017 08 9;78:114-122. Epub 2017 May 9.

Dept. of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.

Mounting evidence suggests that depression represents a risk factor and an early manifestation of Alzheimer's disease (AD). Neuropsychiatric symptoms may derive from neurobiological changes in specific brain areas and may be considered prodromal of dementia. We have previously reported the depressive-like profile in rats receiving a single intracerebroventricular injection of soluble amyloid beta protein (ßA). Here, we verified the effect of different classes of antidepressants on the ßA-induced depressive behavior and on cortical monoamine levels. To these purposes, the forced swimming test was performed and cortical levels of serotonin (5-HT) and noradrenaline (NA) were quantified by high performance liquid chromatography (HPLC). We found that acute fluoxetine (20mg/kg, s.c.), reboxetine (10mg/kg, s.c.), and ketamine (15mg/kg, i.p.) significantly reduced the immobility in ßA-treated rats compared to controls. Fluoxetine and reboxetine reversed 5-HT reduction, while βA-induced NA increase was further enhanced by all treatments. Treatments with fluoxetine, reboxetine and ketamine were able to revert soluble ßA-induced decrease of cortical BDNF levels, while only fluoxetine and ketamine, but not reboxetine, had the same effects on cortical NGF expression. Moreover, plasma soluble ßA-levels were lowered by fluoxetine, but not reboxetine and ketamine, treatments. Our data suggest that different classes of antidepressants yield a short-acting effect on rat soluble ßA-induced depressive profile. Thus, we hypothesize a novel common mechanism of action of these drugs also based upon a "ßA lowering" effect. Although further investigations are still needed, our study might open a new scenario for unravelling the molecular antidepressant mechanisms of these drugs.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.pnpbp.2017.05.004DOI Listing
August 2017

Chlorella sorokiniana Extract Improves Short-Term Memory in Rats.

Molecules 2016 Sep 29;21(10). Epub 2016 Sep 29.

Department of Clinical and Experimental Medicine, University of Foggia, Foggia 71121, Italy.

Increasing evidence shows that eukaryotic microalgae and, in particular, the green microalga , can be used as natural sources to obtain a whole variety of compounds, such as omega (ω)-3 and ω-6 polyunsatured fatty acids (PUFAs). Although either beneficial or toxic effects of have been mainly attributed to its specific ω-3 and ω-6 PUFAs content, the underlying molecular pathways remain to be elucidated yet. Here, we investigate the effects of an acute oral administration of a lipid extract of , containing mainly ω-3 and ω-6 PUFAs, on cognitive, emotional and social behaviour in rats, analysing possible underlying neurochemical alterations. Our results showed improved short-term memory in -treated rats compared to controls, without any differences in exploratory performance, locomotor activity, anxiety profile and depressive-like behaviour. On the other hand, while the social behaviour of -treated animals was significantly decreased, no effects on aggressivity were observed. Neurochemical investigations showed region-specific effects, consisting in an elevation of noradrenaline (NA) and serotonin (5-HT) content in hippocampus, but not in the prefrontal cortex and striatum. In conclusion, our results point towards a beneficial effect of extract on short-term memory, but also highlight the need of caution in the use of this natural supplement due to its possible masked toxic effects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/molecules21101311DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274193PMC
September 2016

Chronic Psychosocial Stress Impairs Bone Homeostasis: A Study in the Social Isolation Reared Rat.

Front Pharmacol 2016 8;7:152. Epub 2016 Jun 8.

Department of Experimental and Clinical Medicine, University of Foggia Foggia, Italy.

Chronic psychosocial stress is a key player in the onset and aggravation of mental diseases, including psychosis. Although a strong association between this psychiatric condition and other medical co-morbidities has been recently demonstrated, few data on the link between psychosis and bone homeostasis are actually available. The aim of this study was to investigate whether chronic psychosocial stress induced by 4 or 7 weeks of social isolation in drug-naïve male Wistar rats could alter bone homeostasis in terms of bone thickness, mineral density and content, as well as markers of bone formation and resorption (sclerostin, cathepsin K, and CTX-I). We found that bone mineral density was increased in rats exposed to 7 weeks of social isolation, while no differences were detected in bone mineral content and area. Moreover, 7 weeks of social isolation lead to increase of femur thickness with respect to controls, suggesting the development of a hyperostosis condition. Isolated rats showed no changes in sclerostin levels, a marker of bone formation, compared to grouped animals. Conversely, bone resorption markers were significantly altered after 7 weeks of social isolation in terms of decrease in cathepsin K and increase of CTX-I. No alterations were found after 4 weeks of isolation rearing. Our observations suggest that chronic psychosocial stress might affect bone homeostasis, more likely independently from drug treatment. Thus, the social isolation model might help to identify possible new therapeutic targets to treat the burden of chronic psychosocial stress and to attempt alternative therapy choices.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fphar.2016.00152DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896906PMC
July 2016

Lifelong Nutritional Omega-3 Deficiency Evokes Depressive-Like State Through Soluble Beta Amyloid.

Mol Neurobiol 2017 04 29;54(3):2079-2089. Epub 2016 Feb 29.

Physiology and Pharmacology, La Sapienza, University of Rome, Rome, Italy.

Recent evidence pointed out that the prevalence of depression has reached epidemic proportions in last decades. This increase has been linked to many environmental factors, among these the influence of dietary factors has gained great attention. In particular, it has been reported that low n-3 polyunsaturated fatty acid (n-3 PUFA) intake in diet is correlated to the development of depressive and anxiety-like symptoms. Furthermore, maternal malnutrition is a widely accepted risk factor for developing mental illness in later adulthood; among others, depression has been strongly associated to this event. On the other hand, we have previously found that acute intracerebral injection of the soluble beta amyloid 1-42 (Aβ) peptide induces a depressive-like behavior in rats, associated to altered hypothalamic-pituitary-adrenal (HPA) axis activation and reduced cortical serotonin and neurotrophin levels. The aim of the present work was to study the effect of pre- and post-natal (5 weeks post-weaning) exposure to diets differently enriched in n-3, n-6, as well as n-6/n-3 PUFA balanced, on immobility time displayed on the forced swimming test (FST), along with neuroendocrine quantification in offspring rats. Results showed that n-6 PUFA-enriched diet increased depressive- and anxiety-like behaviors, as shown by the elevation in the immobility time in the FST test and self-grooming in the open field test. Those effects were accompanied by reduced cortical serotonin, high plasmatic corticosterone and hypothalamic corticotropin-releasing factor levels. Finally, enhanced plasmatic Aβ levels after n-6 PUFA diet and reduced plasmatic Aβ levels after n-3 PUFA were found. Taken together, our data indicate that Aβ might be crucially involved in behavioral alterations found after n-6 rich PUFA diet and strongly endorse the protective role of n-3 and the detrimental effect of improper n-6 PUFA diet consumption.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12035-016-9809-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355522PMC
April 2017

Early Loss of Blood-Brain Barrier Integrity Precedes NOX2 Elevation in the Prefrontal Cortex of an Animal Model of Psychosis.

Mol Neurobiol 2017 04 24;54(3):2031-2044. Epub 2016 Feb 24.

Department of Physiology and Pharmacology, "Sapienza", University of Rome, Rome, Italy.

The social isolation rearing of young adult rats is a model of psychosocial stress and provides a nonpharmacological tool to study alterations reminiscent of symptoms seen in psychosis. We have previously demonstrated that social isolation in rats leads to increased oxidative stress and to cerebral NOX2 elevations. Here, we investigated early alterations in mRNA expression leading to increased NOX2 in the brain. Rats were exposed to a short period of social isolation (1 week) and real-time polymerase chain reaction (PCR) for mRNA expression of genes involved in blood-brain barrier (BBB) formation and integrity (ORLs, Vof 21 and Vof 16, Leng8, Vnr1, and Trank 1 genes) was performed. Real-time PCR experiments, immunohistochemistry, and Western blotting analysis showed an increased expression of these genes and related proteins in isolated rats with respect to control animals. The expression of specific markers of BBB integrity, such as matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), occludin 1, and plasmalemmal vesicle associated protein-1 (PV-1), was also significantly altered after 1 week of social isolation. BBB permeability, evaluated by quantification of Evans blue dye extravasation, as well as interstitial fluid, was significantly increased in rats isolated for 1 week with respect to controls. Isolation-induced BBB disruption was also accompanied by a significant increase of Interleukin 6 (IL-6) expression. Conversely, no differences in NOX2 levels were detected at this time point. Our study demonstrates that BBB disruption precedes NOX2 elevations in the brain. These results provide new insights in the interplay of mechanisms linking psychosocial stress to early oxidative stress in the brain, disruption of the BBB, and the development of mental disorders.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12035-016-9791-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355521PMC
April 2017

Effects of anabolic-androgens on brain reward function.

Front Neurosci 2015 26;9:295. Epub 2015 Aug 26.

Department of Clinical and Experimental Medicine, University of Foggia Foggia, Italy.

Androgens are mainly prescribed to treat several diseases caused by testosterone deficiency. However, athletes try to promote muscle growth by manipulating testosterone levels or assuming androgen anabolic steroids (AAS). These substances were originally synthesized to obtain anabolic effects greater than testosterone. Although AAS are rarely prescribed compared to testosterone, their off-label utilization is very wide. Furthermore, combinations of different steroids and doses generally higher than those used in therapy are common. Symptoms of the chronic use of supra-therapeutic doses of AAS include anxiety, depression, aggression, paranoia, distractibility, confusion, amnesia. Interestingly, some studies have shown that AAS elicited electroencephalographic changes similar to those observed with amphetamine abuse. The frequency of side effects is higher among AAS abusers, with psychiatric complications such as labile mood, lack of impulse control and high violence. On the other hand, AAS addiction studies are complex because data collection is very difficult due to the subjects' reticence and can be biased by many variables, including physical exercise, that alter the reward system. Moreover, it has been reported that AAS may imbalance neurotransmitter systems involved in the reward process, leading to increased sensitivity toward opioid narcotics and central stimulants. The goal of this article is to review the literature on steroid abuse and changes to the reward system in preclinical and clinical studies.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fnins.2015.00295DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549565PMC
September 2015

Comparison of PM10 concentrations and metal content in three different sites of the Venice Lagoon: an analysis of possible aerosol sources.

J Environ Sci (China) 2012 ;24(11):1954-65

Institute of Atmospheric Sciences and Climate, ISAC-CNR, Lecce, Italy.

The Venice Lagoon is exposed to atmospheric pollutants from industrial activities, thermoelectric power plants, petrochemical plants, incinerator, domestic heating, ship traffic, glass factories and vehicular emissions on the mainland. In 2005, construction began on the mobile dams (MOSE), one dam for each channel connecting the lagoon to the Adriatic Sea as a barrier against high tide. These construction works could represent an additional source of pollutants. PM10 samples were taken on random days between 2007 and 2010 at three different sites: Punta Sabbioni, Chioggia and Malamocco, located near the respective dam construction worksites. Chemical analyses of V, Cr, Fe, Co, Ni, Cu, Zn, As, Mo, Cd, Sb, Tl and Pb in PM10 samples were performed by Inductively coupled plasma-quadrupole mass spectrometry (ICP-QMS) and results were used to identify the main aerosol sources. The correlation of measured data with meteorology, and source apportionment, failed to highlight a contribution specifically associated to the emissions of the MOSE construction works. The comparison of the measurements at the three sites showed a substantial homogeneity of metal concentrations in the area. Source apportionment with principal component analysis (PCA) and positive matrix factorization (PMF) showed that a four principal factors model could describe the sources of metals in PM10. Three of them were assigned to specific sources in the area and one was characterised as a source of mixed origin (anthropogenic and crustal). A specific anthropogenic source of PM10 rich in Ni and Cr, active at the Chioggia site, was also identified.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/s1001-0742(11)61027-9DOI Listing
May 2013