TY  - CONF
AU  - Laketa, Danijela
AU  - Manojlović-Stojanoski, Milica
AU  - Lavrnja, Irena
AU  - Stevanović, Ivana
AU  - Trifunović, Svetlana
AU  - Ristić, Nataša
AU  - Nestorović, Nataša
AU  - Sévigny, Jean
AU  - Nedeljković, Nadežda
PY  - 2021
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6209
AB  - To accelerate organ maturation and prevent complications due to preterm birth, antenatal treatment with
synthetic glucocorticoids (GCs – dexamethasone or betamethasone) is usually given between the 24th
and 34th week of pregnancy to women at risk of delivery within the next seven days [1]. Despite recommendations,
repeat courses of antenatal GCs are frequently given, although excessive GC stimulation may
exert adverse neurodevelopmental effects [1]. The purinergic system is essential for neurodevelopment
[2]. Extracellular purine levels are regulated by ectonucleotidases, with ectonucleoside triphosphate diphosphohydrolase
1 (NTPDase1/CD39) and ecto-5ʹ-nucleotidase (e5ʹNT/CD73), abundant in the CNS,
which jointly hydrolyze ATP to adenosine. Both ectonucleotidases are also involved in cell adhesion
and migration [3]. We aimed to explore the effects of antenatal dexamethasone (DEX) treatment on the
expression and enzymatic activity of NTPDase1/e5ʹNT tandem in the rat fetal brain. Wistar rat dams were
treated with 0.5 mg/kg DEX, at gestation day (GD) 16, 17, and 18. We found sex-specific male-biased
upregulation of CD39 and CD73 mRNA and protein abundances, and an increase in the corresponding enzymatic activities in the rat fetal brain at GD21, induced by antenatal DEX treatment. Observed changes
indicate a possible decrease in P2, and an increase in P1 purinergic receptors-mediated signaling, as
well as a potential decrease in migration of progenitor cells, particularly pronounced in the brain of male
fetuses. Together, sex-dependent induction of CD39 and CD73 might interfere with neurodevelopmental
processes, thus contributing to adverse effects of antenatal DEX treatment, especially in males.
PB  - Federation of European Neuroscience Societies
C3  - Book of Abstracts: Virtual FENS Regional Meeting 2021; 2021 Aug 25-27; Krakow, Poland
T1  - NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 are Upregulated in a Sex-specific fashion in the Rat Fetal Brain After Repeated Antenatal Dexamethasone Treatment
SP  - 192
EP  - 193
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6209
ER  - 

@conference{
author = "Laketa, Danijela and Manojlović-Stojanoski, Milica and Lavrnja, Irena and Stevanović, Ivana and Trifunović, Svetlana and Ristić, Nataša and Nestorović, Nataša and Sévigny, Jean and Nedeljković, Nadežda",
year = "2021",
abstract = "To accelerate organ maturation and prevent complications due to preterm birth, antenatal treatment with
synthetic glucocorticoids (GCs – dexamethasone or betamethasone) is usually given between the 24th
and 34th week of pregnancy to women at risk of delivery within the next seven days [1]. Despite recommendations,
repeat courses of antenatal GCs are frequently given, although excessive GC stimulation may
exert adverse neurodevelopmental effects [1]. The purinergic system is essential for neurodevelopment
[2]. Extracellular purine levels are regulated by ectonucleotidases, with ectonucleoside triphosphate diphosphohydrolase
1 (NTPDase1/CD39) and ecto-5ʹ-nucleotidase (e5ʹNT/CD73), abundant in the CNS,
which jointly hydrolyze ATP to adenosine. Both ectonucleotidases are also involved in cell adhesion
and migration [3]. We aimed to explore the effects of antenatal dexamethasone (DEX) treatment on the
expression and enzymatic activity of NTPDase1/e5ʹNT tandem in the rat fetal brain. Wistar rat dams were
treated with 0.5 mg/kg DEX, at gestation day (GD) 16, 17, and 18. We found sex-specific male-biased
upregulation of CD39 and CD73 mRNA and protein abundances, and an increase in the corresponding enzymatic activities in the rat fetal brain at GD21, induced by antenatal DEX treatment. Observed changes
indicate a possible decrease in P2, and an increase in P1 purinergic receptors-mediated signaling, as
well as a potential decrease in migration of progenitor cells, particularly pronounced in the brain of male
fetuses. Together, sex-dependent induction of CD39 and CD73 might interfere with neurodevelopmental
processes, thus contributing to adverse effects of antenatal DEX treatment, especially in males.",
publisher = "Federation of European Neuroscience Societies",
journal = "Book of Abstracts: Virtual FENS Regional Meeting 2021; 2021 Aug 25-27; Krakow, Poland",
title = "NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 are Upregulated in a Sex-specific fashion in the Rat Fetal Brain After Repeated Antenatal Dexamethasone Treatment",
pages = "192-193",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6209"
}

Laketa, D., Manojlović-Stojanoski, M., Lavrnja, I., Stevanović, I., Trifunović, S., Ristić, N., Nestorović, N., Sévigny, J.,& Nedeljković, N.. (2021). NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 are Upregulated in a Sex-specific fashion in the Rat Fetal Brain After Repeated Antenatal Dexamethasone Treatment. in Book of Abstracts: Virtual FENS Regional Meeting 2021; 2021 Aug 25-27; Krakow, Poland
Federation of European Neuroscience Societies., 192-193.
https://hdl.handle.net/21.15107/rcub_ibiss_6209

Laketa D, Manojlović-Stojanoski M, Lavrnja I, Stevanović I, Trifunović S, Ristić N, Nestorović N, Sévigny J, Nedeljković N. NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 are Upregulated in a Sex-specific fashion in the Rat Fetal Brain After Repeated Antenatal Dexamethasone Treatment. in Book of Abstracts: Virtual FENS Regional Meeting 2021; 2021 Aug 25-27; Krakow, Poland. 2021;:192-193.
https://hdl.handle.net/21.15107/rcub_ibiss_6209 .

Laketa, Danijela, Manojlović-Stojanoski, Milica, Lavrnja, Irena, Stevanović, Ivana, Trifunović, Svetlana, Ristić, Nataša, Nestorović, Nataša, Sévigny, Jean, Nedeljković, Nadežda, "NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 are Upregulated in a Sex-specific fashion in the Rat Fetal Brain After Repeated Antenatal Dexamethasone Treatment" in Book of Abstracts: Virtual FENS Regional Meeting 2021; 2021 Aug 25-27; Krakow, Poland (2021):192-193,
https://hdl.handle.net/21.15107/rcub_ibiss_6209 .

TY  - JOUR
AU  - Dejanovic, Bratislav
AU  - Stevanovic, Ivana
AU  - Ninkovic, Milica
AU  - Stojanovic, Ivana
AU  - Lavrnja, Irena
AU  - Radicevic, Tatjana
AU  - Pavlovic, Milos
PY  - 2016
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1986
AB  - This study was conducted to investigate whether agmatine (AGM) provides
   protection against oxidative stress induced by treatment with
   chlorpromazine (CPZ) in Wistar rats. In addition, the role of reactive
   oxygen species and efficiency of antioxidant protection in the brain
   homogenates of forebrain cortexes prepared 48 h after treatment were
   investigated. Chlorpromazine was applied intraperitoneally (i.p.) in
   single dose of 38.7 mg/kg body weight (BW) The second group was treated
   with both CPZ and AGM (75 mg/kg BW). The control group was treated with
   0.9\% saline solution in the same manner. All tested compounds were
   administered i.p. in a single dose. Rats were sacrificed by decapitation
   48 h after treatment Treatment with AGM significantly attenuated the
   oxidative stress parameters and restored antioxidant capacity in the
   forebrain cortex. The data indicated that i.p. administered AGM exerted
   antioxidant action in CPZ-treated animals. Moreover, reactive astrocytes
   and microglia may contribute to secondary nerve-cell damage and
   participate in the balance of destructive vs. protective actions
   involved in the pathogenesis after poisoning.
T2  - Journal of Veterinary Science
T1  - Agmatine protection against chlorpromazine-induced forebrain cortex
 injury in rats
IS  - 1
VL  - 17
DO  - 10.4142/jvs.2016.17.1.53
SP  - 53
EP  - 61
ER  - 

@article{
author = "Dejanovic, Bratislav and Stevanovic, Ivana and Ninkovic, Milica and Stojanovic, Ivana and Lavrnja, Irena and Radicevic, Tatjana and Pavlovic, Milos",
year = "2016",
abstract = "This study was conducted to investigate whether agmatine (AGM) provides
   protection against oxidative stress induced by treatment with
   chlorpromazine (CPZ) in Wistar rats. In addition, the role of reactive
   oxygen species and efficiency of antioxidant protection in the brain
   homogenates of forebrain cortexes prepared 48 h after treatment were
   investigated. Chlorpromazine was applied intraperitoneally (i.p.) in
   single dose of 38.7 mg/kg body weight (BW) The second group was treated
   with both CPZ and AGM (75 mg/kg BW). The control group was treated with
   0.9\% saline solution in the same manner. All tested compounds were
   administered i.p. in a single dose. Rats were sacrificed by decapitation
   48 h after treatment Treatment with AGM significantly attenuated the
   oxidative stress parameters and restored antioxidant capacity in the
   forebrain cortex. The data indicated that i.p. administered AGM exerted
   antioxidant action in CPZ-treated animals. Moreover, reactive astrocytes
   and microglia may contribute to secondary nerve-cell damage and
   participate in the balance of destructive vs. protective actions
   involved in the pathogenesis after poisoning.",
journal = "Journal of Veterinary Science",
title = "Agmatine protection against chlorpromazine-induced forebrain cortex
 injury in rats",
number = "1",
volume = "17",
doi = "10.4142/jvs.2016.17.1.53",
pages = "53-61"
}

Dejanovic, B., Stevanovic, I., Ninkovic, M., Stojanovic, I., Lavrnja, I., Radicevic, T.,& Pavlovic, M.. (2016). Agmatine protection against chlorpromazine-induced forebrain cortex
 injury in rats. in Journal of Veterinary Science, 17(1), 53-61.
https://doi.org/10.4142/jvs.2016.17.1.53

Dejanovic B, Stevanovic I, Ninkovic M, Stojanovic I, Lavrnja I, Radicevic T, Pavlovic M. Agmatine protection against chlorpromazine-induced forebrain cortex
 injury in rats. in Journal of Veterinary Science. 2016;17(1):53-61.
doi:10.4142/jvs.2016.17.1.53 .

Dejanovic, Bratislav, Stevanovic, Ivana, Ninkovic, Milica, Stojanovic, Ivana, Lavrnja, Irena, Radicevic, Tatjana, Pavlovic, Milos, "Agmatine protection against chlorpromazine-induced forebrain cortex
 injury in rats" in Journal of Veterinary Science, 17, no. 1 (2016):53-61,
https://doi.org/10.4142/jvs.2016.17.1.53 . .

TY  - JOUR
AU  - Božić, Iva
AU  - Savić, Danijela
AU  - Stevanovic, Ivana
AU  - Peković, Sanja
AU  - Nedeljkovic, Nadezda
AU  - Lavrnja, Irena
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2363
AB  - Chronic microglial activation and resulting sustained neuroinflammatory
   reaction are generally associated with neurodegeneration. Activated
   microglia acquires proinflammatory cellular profile that generates
   oxidative burst. Their persistent activation exacerbates inflammation,
   which damages healthy neurons via cytotoxic mediators, such as
   superoxide radical anion and nitric oxide. In our recent study, we have
   shown that benfotiamine (S-benzoylthiamine 0-monophosphate) possesses
   anti-inflammatory effects. Here, the effects of benfotiamine on the
   pro-oxidative component of activity of LPS-stimulated BV -2 cells were
   investigated. The activation of microglia was accompanied by
   upregulation of intracellular antioxidative defense, which was further
   promoted in the presence of benfotiamine. Namely, activated microglia
   exposed to non-cytotoxic doses of benfotiamine showed increased levels
   and activities of hydrogen peroxide- and superoxide removing enzymes
   catalase and glutathione system, and superoxide dismutase. In addition,
   benfotiamine showed the capacity to directly scavenge superoxide radical
   anion. As a consequence, benfotiamine suppressed the activation of
   microglia and provoked a decrease in NO and O-center dot(2)- production
   and lipid peroxidation. In conclusion, benfotiamine might silence
   pro-oxidative activity of microglia to alleviate/prevent oxidative
   damage of neighboring CNS cells.
T2  - Frontiers in Cellular Neuroscience
T1  - Benfotiamine upregulates antioxidative system in activated BV-2
 microglia cells
IS  - 351
VL  - 9
DO  - 10.3389/fncel.2015.00351
ER  - 

@article{
author = "Božić, Iva and Savić, Danijela and Stevanovic, Ivana and Peković, Sanja and Nedeljkovic, Nadezda and Lavrnja, Irena",
year = "2015",
abstract = "Chronic microglial activation and resulting sustained neuroinflammatory
   reaction are generally associated with neurodegeneration. Activated
   microglia acquires proinflammatory cellular profile that generates
   oxidative burst. Their persistent activation exacerbates inflammation,
   which damages healthy neurons via cytotoxic mediators, such as
   superoxide radical anion and nitric oxide. In our recent study, we have
   shown that benfotiamine (S-benzoylthiamine 0-monophosphate) possesses
   anti-inflammatory effects. Here, the effects of benfotiamine on the
   pro-oxidative component of activity of LPS-stimulated BV -2 cells were
   investigated. The activation of microglia was accompanied by
   upregulation of intracellular antioxidative defense, which was further
   promoted in the presence of benfotiamine. Namely, activated microglia
   exposed to non-cytotoxic doses of benfotiamine showed increased levels
   and activities of hydrogen peroxide- and superoxide removing enzymes
   catalase and glutathione system, and superoxide dismutase. In addition,
   benfotiamine showed the capacity to directly scavenge superoxide radical
   anion. As a consequence, benfotiamine suppressed the activation of
   microglia and provoked a decrease in NO and O-center dot(2)- production
   and lipid peroxidation. In conclusion, benfotiamine might silence
   pro-oxidative activity of microglia to alleviate/prevent oxidative
   damage of neighboring CNS cells.",
journal = "Frontiers in Cellular Neuroscience",
title = "Benfotiamine upregulates antioxidative system in activated BV-2
 microglia cells",
number = "351",
volume = "9",
doi = "10.3389/fncel.2015.00351"
}

Božić, I., Savić, D., Stevanovic, I., Peković, S., Nedeljkovic, N.,& Lavrnja, I.. (2015). Benfotiamine upregulates antioxidative system in activated BV-2
 microglia cells. in Frontiers in Cellular Neuroscience, 9(351).
https://doi.org/10.3389/fncel.2015.00351

Božić I, Savić D, Stevanovic I, Peković S, Nedeljkovic N, Lavrnja I. Benfotiamine upregulates antioxidative system in activated BV-2
 microglia cells. in Frontiers in Cellular Neuroscience. 2015;9(351).
doi:10.3389/fncel.2015.00351 .

Božić, Iva, Savić, Danijela, Stevanovic, Ivana, Peković, Sanja, Nedeljkovic, Nadezda, Lavrnja, Irena, "Benfotiamine upregulates antioxidative system in activated BV-2
 microglia cells" in Frontiers in Cellular Neuroscience, 9, no. 351 (2015),
https://doi.org/10.3389/fncel.2015.00351 . .

TY  - JOUR
AU  - Jelenković, Ankica V.
AU  - Jovanovic, Marina D.
AU  - Stevanovic, Ivana
AU  - Petronijevic, Natasa
AU  - Bokonjic, Dubravko
AU  - Zivkovic, Jelena
AU  - Igic, Rajko
PY  - 2014
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2306
AB  - Aluminium may have an important role in the
   aetiology/pathogenesis/precipitation of Alzheimer's disease. Because
   green tea (Camellia sinensis L.) reportedly has health-promoting effects
   in the central nervous system, we evaluated the effects of green tea
   leaf extract (GTLE) on aluminium chloride (AlCl3) neurotoxicity in rats.
   All solutions were injected into the cornu ammonis region 1 hippocampal
   region. We measured the performance of active avoidance (AA) tasks,
   various enzyme activities and total glutathione content (TGC) in the
   forebrain cortex (FbC), striatum, basal forebrain (BFb), hippocampus,
   brain stem and cerebellum. AlCl3 markedly reduced AA performance and
   activities of cytochrome c oxidase (COX) and acetylcholinesterase (AChE)
   in all regions. It decreased TGC in the FbC, striatum, BFb, hippocampus,
   brain stem and cerebellum, and increased superoxide dismutase activity
   in the FbC, cerebellum and BFb. GTLE pretreatment completely reversed
   the damaging effects of AlCl3 on AA and superoxide dismutase activity,
   markedly corrected COX and AChE activities, and moderately improved TGC.
   GTLE alone increased COX and AChE activities in almost all regions. GTLE
   reduces AlCl3 neurotoxicity probably via antioxidative effects and
   improves mitochondrial and cholinergic synaptic functions through the
   actions of (-)-epigallocatechin gallate and (-)-epicatechin, compounds
   most abundantly found in GTLE. Our results suggest that green tea might
   be beneficial in Alzheimer's disease. Copyright (c) 2013 John Wiley \&
   Sons, Ltd.
T2  - Phytotherapy Research
T1  - Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium
 Chloride in Rats
IS  - 1
VL  - 28
DO  - 10.1002/ptr.4962
SP  - 82
EP  - 87
ER  - 

@article{
author = "Jelenković, Ankica V. and Jovanovic, Marina D. and Stevanovic, Ivana and Petronijevic, Natasa and Bokonjic, Dubravko and Zivkovic, Jelena and Igic, Rajko",
year = "2014",
abstract = "Aluminium may have an important role in the
   aetiology/pathogenesis/precipitation of Alzheimer's disease. Because
   green tea (Camellia sinensis L.) reportedly has health-promoting effects
   in the central nervous system, we evaluated the effects of green tea
   leaf extract (GTLE) on aluminium chloride (AlCl3) neurotoxicity in rats.
   All solutions were injected into the cornu ammonis region 1 hippocampal
   region. We measured the performance of active avoidance (AA) tasks,
   various enzyme activities and total glutathione content (TGC) in the
   forebrain cortex (FbC), striatum, basal forebrain (BFb), hippocampus,
   brain stem and cerebellum. AlCl3 markedly reduced AA performance and
   activities of cytochrome c oxidase (COX) and acetylcholinesterase (AChE)
   in all regions. It decreased TGC in the FbC, striatum, BFb, hippocampus,
   brain stem and cerebellum, and increased superoxide dismutase activity
   in the FbC, cerebellum and BFb. GTLE pretreatment completely reversed
   the damaging effects of AlCl3 on AA and superoxide dismutase activity,
   markedly corrected COX and AChE activities, and moderately improved TGC.
   GTLE alone increased COX and AChE activities in almost all regions. GTLE
   reduces AlCl3 neurotoxicity probably via antioxidative effects and
   improves mitochondrial and cholinergic synaptic functions through the
   actions of (-)-epigallocatechin gallate and (-)-epicatechin, compounds
   most abundantly found in GTLE. Our results suggest that green tea might
   be beneficial in Alzheimer's disease. Copyright (c) 2013 John Wiley \&
   Sons, Ltd.",
journal = "Phytotherapy Research",
title = "Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium
 Chloride in Rats",
number = "1",
volume = "28",
doi = "10.1002/ptr.4962",
pages = "82-87"
}

Jelenković, A. V., Jovanovic, M. D., Stevanovic, I., Petronijevic, N., Bokonjic, D., Zivkovic, J.,& Igic, R.. (2014). Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium
 Chloride in Rats. in Phytotherapy Research, 28(1), 82-87.
https://doi.org/10.1002/ptr.4962

Jelenković AV, Jovanovic MD, Stevanovic I, Petronijevic N, Bokonjic D, Zivkovic J, Igic R. Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium
 Chloride in Rats. in Phytotherapy Research. 2014;28(1):82-87.
doi:10.1002/ptr.4962 .

Jelenković, Ankica V., Jovanovic, Marina D., Stevanovic, Ivana, Petronijevic, Natasa, Bokonjic, Dubravko, Zivkovic, Jelena, Igic, Rajko, "Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium
 Chloride in Rats" in Phytotherapy Research, 28, no. 1 (2014):82-87,
https://doi.org/10.1002/ptr.4962 . .