Labudović-Borović, Milica

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  • Labudović-Borović, Milica (4)
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Author's Bibliography

The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis

Nastić, Katarina; Pecikoza, Uroš; Labudović-Borović, Milica; Kotur-Stevuljević, Jelena; Micov, Ana; Jovanović, Aleksandar; Tomić, Maja; Stepanović-Petrović, Radica

(Elsevier Masson, 2023)

TY  - JOUR
AU  - Nastić, Katarina
AU  - Pecikoza, Uroš
AU  - Labudović-Borović, Milica
AU  - Kotur-Stevuljević, Jelena
AU  - Micov, Ana
AU  - Jovanović, Aleksandar
AU  - Tomić, Maja
AU  - Stepanović-Petrović, Radica
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5018
AB  - Osteoarthritis represents a leading cause of disability with limited treatment options. Furthermore, it is frequently accompanied by cardiovascular and cognitive disorders, which can be exacerbated by osteoarthritis or drugs used for its treatment. Here, we examined the behavioral and cardiac effects of the novel antidepressant vortioxetine in an osteoarthritis model, and compared them to duloxetine (an established osteoarthritis treatment). Osteoarthritis was induced in male and female rats with an intraarticular sodium-monoiodoacetate injection. Antidepressants were orally administered for 28 days following induction. During this period the acetone, burrowing and novel-object-recognition tests (NORT) were used to assess the effects of antidepressants on pain hypersensitivity (cold allodynia), animal well-being and cognitive performance, respectively. Following behavioral experiments, heart muscles were collected for assessment of redox status/histology. Antidepressant treatment dose-dependently reduced cold allodynia in rats with osteoarthritis. Duloxetine (but not vortioxetine) depressed burrowing behavior in osteoarthritic rats in a dose-related manner. Osteoarthritis induction reduced cognitive performance in NORT, which was dose-dependently alleviated by vortioxetine (duloxetine improved performance only in female rats). Furthermore, duloxetine (but not vortioxetine) increased oxidative stress parameters in the heart muscles of female (but not male) rats and induced histological changes in cardiomyocytes indicative of oxidative damage. Vortioxetine displayed comparable efficacy to duloxetine in reducing pain hypersensitivity. Furthermore, vortioxetine (unlike duloxetine) dose-dependently improved cognitive performance and had no adverse effect on burrowing behavior (animal surrogate of well-being) and cardiac redox status/histology. Our results indicate that vortioxetine could be a potential osteoarthritis treatment (with better characteristics compared to duloxetine).
PB  - Elsevier Masson
T2  - Biomedicine and Pharmacotherapy
T1  - The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis
VL  - 166
DO  - 10.1016/j.biopha.2023.115360
ER  - 
@article{
author = "Nastić, Katarina and Pecikoza, Uroš and Labudović-Borović, Milica and Kotur-Stevuljević, Jelena and Micov, Ana and Jovanović, Aleksandar and Tomić, Maja and Stepanović-Petrović, Radica",
year = "2023",
abstract = "Osteoarthritis represents a leading cause of disability with limited treatment options. Furthermore, it is frequently accompanied by cardiovascular and cognitive disorders, which can be exacerbated by osteoarthritis or drugs used for its treatment. Here, we examined the behavioral and cardiac effects of the novel antidepressant vortioxetine in an osteoarthritis model, and compared them to duloxetine (an established osteoarthritis treatment). Osteoarthritis was induced in male and female rats with an intraarticular sodium-monoiodoacetate injection. Antidepressants were orally administered for 28 days following induction. During this period the acetone, burrowing and novel-object-recognition tests (NORT) were used to assess the effects of antidepressants on pain hypersensitivity (cold allodynia), animal well-being and cognitive performance, respectively. Following behavioral experiments, heart muscles were collected for assessment of redox status/histology. Antidepressant treatment dose-dependently reduced cold allodynia in rats with osteoarthritis. Duloxetine (but not vortioxetine) depressed burrowing behavior in osteoarthritic rats in a dose-related manner. Osteoarthritis induction reduced cognitive performance in NORT, which was dose-dependently alleviated by vortioxetine (duloxetine improved performance only in female rats). Furthermore, duloxetine (but not vortioxetine) increased oxidative stress parameters in the heart muscles of female (but not male) rats and induced histological changes in cardiomyocytes indicative of oxidative damage. Vortioxetine displayed comparable efficacy to duloxetine in reducing pain hypersensitivity. Furthermore, vortioxetine (unlike duloxetine) dose-dependently improved cognitive performance and had no adverse effect on burrowing behavior (animal surrogate of well-being) and cardiac redox status/histology. Our results indicate that vortioxetine could be a potential osteoarthritis treatment (with better characteristics compared to duloxetine).",
publisher = "Elsevier Masson",
journal = "Biomedicine and Pharmacotherapy",
title = "The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis",
volume = "166",
doi = "10.1016/j.biopha.2023.115360"
}
Nastić, K., Pecikoza, U., Labudović-Borović, M., Kotur-Stevuljević, J., Micov, A., Jovanović, A., Tomić, M.,& Stepanović-Petrović, R.. (2023). The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis. in Biomedicine and Pharmacotherapy
Elsevier Masson., 166.
https://doi.org/10.1016/j.biopha.2023.115360
Nastić K, Pecikoza U, Labudović-Borović M, Kotur-Stevuljević J, Micov A, Jovanović A, Tomić M, Stepanović-Petrović R. The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis. in Biomedicine and Pharmacotherapy. 2023;166.
doi:10.1016/j.biopha.2023.115360 .
Nastić, Katarina, Pecikoza, Uroš, Labudović-Borović, Milica, Kotur-Stevuljević, Jelena, Micov, Ana, Jovanović, Aleksandar, Tomić, Maja, Stepanović-Petrović, Radica, "The antidepressant drugs vortioxetine and duloxetine differentially and sex-dependently affect animal well-being, cognitive performance, cardiac redox status and histology in a model of osteoarthritis" in Biomedicine and Pharmacotherapy, 166 (2023),
https://doi.org/10.1016/j.biopha.2023.115360 . .

Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?

Rakočević, Jelena; Dobrić, Milan; Labudović-Borović, Milica; Milutinović, Katarina; Milenković, Sanela; Tomašević, Miloje

(IMR Press Limited, 2023)

TY  - JOUR
AU  - Rakočević, Jelena
AU  - Dobrić, Milan
AU  - Labudović-Borović, Milica
AU  - Milutinović, Katarina
AU  - Milenković, Sanela
AU  - Tomašević, Miloje
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4520
AB  - Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease.
PB  - IMR Press Limited
T2  - Reviews in Cardiovascular Medicine
T1  - Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?
VL  - 24
IS  - 1
DO  - 10.31083/j.rcm2401010
ER  - 
@article{
author = "Rakočević, Jelena and Dobrić, Milan and Labudović-Borović, Milica and Milutinović, Katarina and Milenković, Sanela and Tomašević, Miloje",
year = "2023",
abstract = "Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease.",
publisher = "IMR Press Limited",
journal = "Reviews in Cardiovascular Medicine",
title = "Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?",
volume = "24",
number = "1",
doi = "10.31083/j.rcm2401010"
}
Rakočević, J., Dobrić, M., Labudović-Borović, M., Milutinović, K., Milenković, S.,& Tomašević, M.. (2023). Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?. in Reviews in Cardiovascular Medicine
IMR Press Limited., 24(1).
https://doi.org/10.31083/j.rcm2401010
Rakočević J, Dobrić M, Labudović-Borović M, Milutinović K, Milenković S, Tomašević M. Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?. in Reviews in Cardiovascular Medicine. 2023;24(1).
doi:10.31083/j.rcm2401010 .
Rakočević, Jelena, Dobrić, Milan, Labudović-Borović, Milica, Milutinović, Katarina, Milenković, Sanela, Tomašević, Miloje, "Anti-Inflammatory Therapy in Coronary Artery Disease: Where Do We Stand?" in Reviews in Cardiovascular Medicine, 24, no. 1 (2023),
https://doi.org/10.31083/j.rcm2401010 . .
4
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Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration

Petrović, Jelena; Stanić, Dušanka; Bulat, Zorica; Puskas, Nela; Labudović-Borović, Milica; Batinić, Bojan; Mirković, Duško; Ignjatović, Svetlana; Pešić, Vesna

(Academic Press Inc Elsevier Science, San Diego, 2018)

TY  - JOUR
AU  - Petrović, Jelena
AU  - Stanić, Dušanka
AU  - Bulat, Zorica
AU  - Puskas, Nela
AU  - Labudović-Borović, Milica
AU  - Batinić, Bojan
AU  - Mirković, Duško
AU  - Ignjatović, Svetlana
AU  - Pešić, Vesna
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3042
AB  - Magnesium (Mg), is not only a modulator of the glutamatergic NMDA receptors' affinity, it also prevents HPA axis hyperactivity, thus possibly being implicated in neurobiological features of mood disorders. Further uncovering of molecular mechanisms underlying magnesium's proposed effects is needed due to the recent shift in research of treatment resistant depression (TRD) towards glutamatergic pathways. Here, we applied Mg via drinking water for 28 days (50 mg/kg/day), in ACTH-treated rats, an established animal model of depression resistant to tricyclic antidepressants. Using this model in male rats we measured (1) changes in hippocampal neurogenesis and behavioral alterations, (2) adrenal hormones response to acute stress challenge and (3) levels of biometals involved in regulation of monoamines turnover in rat prefrontal cortex. Our results support beneficial behavioral impact of Mg in TRD model together with increased hippocampal neurogenesis and BDNF expression. Furthermore, Mg prevented ACTH-induced disruption in HPA axis function, by normalizing the levels of plasma ACTH, corticosterone and interleukin-6, and by increasing the peripheral release of adrenaline, noradrenaline and serotonin after the acute stress challenge. Finally, the influence on copper/zinc ratio suggested probable magnesium's involvement in monoamine turnover in PFC. Our findings provide further insights into the possible pathways implicated in the behavioral modulation effects of Mg, as well as its central and peripheral effects in ACTH-induced TRD model. Thus, further investigation of molecular signaling related to the glutamatergic transmission and role of Mg, could reveal prospects to novel treatment strategies that could be of particular importance for patients suffering from TRD.
PB  - Academic Press Inc Elsevier Science, San Diego
T2  - Hormones and Behavior
T1  - Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration
VL  - 105
SP  - 1
EP  - 10
DO  - 10.1016/j.yhbeh.2018.07.003
ER  - 
@article{
author = "Petrović, Jelena and Stanić, Dušanka and Bulat, Zorica and Puskas, Nela and Labudović-Borović, Milica and Batinić, Bojan and Mirković, Duško and Ignjatović, Svetlana and Pešić, Vesna",
year = "2018",
abstract = "Magnesium (Mg), is not only a modulator of the glutamatergic NMDA receptors' affinity, it also prevents HPA axis hyperactivity, thus possibly being implicated in neurobiological features of mood disorders. Further uncovering of molecular mechanisms underlying magnesium's proposed effects is needed due to the recent shift in research of treatment resistant depression (TRD) towards glutamatergic pathways. Here, we applied Mg via drinking water for 28 days (50 mg/kg/day), in ACTH-treated rats, an established animal model of depression resistant to tricyclic antidepressants. Using this model in male rats we measured (1) changes in hippocampal neurogenesis and behavioral alterations, (2) adrenal hormones response to acute stress challenge and (3) levels of biometals involved in regulation of monoamines turnover in rat prefrontal cortex. Our results support beneficial behavioral impact of Mg in TRD model together with increased hippocampal neurogenesis and BDNF expression. Furthermore, Mg prevented ACTH-induced disruption in HPA axis function, by normalizing the levels of plasma ACTH, corticosterone and interleukin-6, and by increasing the peripheral release of adrenaline, noradrenaline and serotonin after the acute stress challenge. Finally, the influence on copper/zinc ratio suggested probable magnesium's involvement in monoamine turnover in PFC. Our findings provide further insights into the possible pathways implicated in the behavioral modulation effects of Mg, as well as its central and peripheral effects in ACTH-induced TRD model. Thus, further investigation of molecular signaling related to the glutamatergic transmission and role of Mg, could reveal prospects to novel treatment strategies that could be of particular importance for patients suffering from TRD.",
publisher = "Academic Press Inc Elsevier Science, San Diego",
journal = "Hormones and Behavior",
title = "Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration",
volume = "105",
pages = "1-10",
doi = "10.1016/j.yhbeh.2018.07.003"
}
Petrović, J., Stanić, D., Bulat, Z., Puskas, N., Labudović-Borović, M., Batinić, B., Mirković, D., Ignjatović, S.,& Pešić, V.. (2018). Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration. in Hormones and Behavior
Academic Press Inc Elsevier Science, San Diego., 105, 1-10.
https://doi.org/10.1016/j.yhbeh.2018.07.003
Petrović J, Stanić D, Bulat Z, Puskas N, Labudović-Borović M, Batinić B, Mirković D, Ignjatović S, Pešić V. Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration. in Hormones and Behavior. 2018;105:1-10.
doi:10.1016/j.yhbeh.2018.07.003 .
Petrović, Jelena, Stanić, Dušanka, Bulat, Zorica, Puskas, Nela, Labudović-Borović, Milica, Batinić, Bojan, Mirković, Duško, Ignjatović, Svetlana, Pešić, Vesna, "Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration" in Hormones and Behavior, 105 (2018):1-10,
https://doi.org/10.1016/j.yhbeh.2018.07.003 . .
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Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats

Petrović, Jelena; Labudović-Borović, Milica; Puškaš, Nela; Stanić, Dušanka; Batinić, Bojan; Plećaš-Solarović, Bosiljka; Pešić, Vesna

(Elsevier Science BV, Amsterdam, 2017)

TY  - CONF
AU  - Petrović, Jelena
AU  - Labudović-Borović, Milica
AU  - Puškaš, Nela
AU  - Stanić, Dušanka
AU  - Batinić, Bojan
AU  - Plećaš-Solarović, Bosiljka
AU  - Pešić, Vesna
PY  - 2017
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2894
PB  - Elsevier Science BV, Amsterdam
C3  - European Neuropsychopharmacology
T1  - Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats
VL  - 27
IS  - Supplement 4
SP  - S765
EP  - S766
DO  - 10.1016/S0924-977X(17)31398-6
ER  - 
@conference{
author = "Petrović, Jelena and Labudović-Borović, Milica and Puškaš, Nela and Stanić, Dušanka and Batinić, Bojan and Plećaš-Solarović, Bosiljka and Pešić, Vesna",
year = "2017",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Neuropsychopharmacology",
title = "Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats",
volume = "27",
number = "Supplement 4",
pages = "S765-S766",
doi = "10.1016/S0924-977X(17)31398-6"
}
Petrović, J., Labudović-Borović, M., Puškaš, N., Stanić, D., Batinić, B., Plećaš-Solarović, B.,& Pešić, V.. (2017). Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats. in European Neuropsychopharmacology
Elsevier Science BV, Amsterdam., 27(Supplement 4), S765-S766.
https://doi.org/10.1016/S0924-977X(17)31398-6
Petrović J, Labudović-Borović M, Puškaš N, Stanić D, Batinić B, Plećaš-Solarović B, Pešić V. Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats. in European Neuropsychopharmacology. 2017;27(Supplement 4):S765-S766.
doi:10.1016/S0924-977X(17)31398-6 .
Petrović, Jelena, Labudović-Borović, Milica, Puškaš, Nela, Stanić, Dušanka, Batinić, Bojan, Plećaš-Solarović, Bosiljka, Pešić, Vesna, "Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats" in European Neuropsychopharmacology, 27, no. Supplement 4 (2017):S765-S766,
https://doi.org/10.1016/S0924-977X(17)31398-6 . .
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