Azotni oksid, neurodegeneracija i Parkinsonova bolest

Džoljić, Eleonora; Nesic, I Zorica; Stojanovic, M Radan; Divac, Nevena; Todorović, Zoran; Vučković, Marijana; Kostić, Smiljana; Prostran, S Milica

doi:10.2298/vsp0510751d

Cited by 4 publications

(10 citation statements)

References 64 publications

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“…Consistent with the primary role of NMDA receptors in driving NO synthesis in the CNS, NMDA receptor overactivity has been reported in numerous neurodegenerative conditions, including HD, AD, PD amyotrophic lateral sclerosis (ALS), as well as in stroke (Džoljić et al, 2005). Recent evidence suggests that neurotoxic mechanisms may play a role in the etiology of PD predominantly.…”

Section: Neurodegenerationmentioning

confidence: 71%

“…Recent evidence suggests that neurotoxic mechanisms may play a role in the etiology of PD predominantly. Likewise, selective nNOS inhibitors exert protection, which suggests that they might be used as novel therapeutic strategies for neuroprotection in PD (Džoljić et al, 2005).…”

Section: Neurodegenerationmentioning

confidence: 99%

“…In practice, if there is a greater transfer of NO from caspase-3 to XIAP, then the latter loses its functionality (Nakamura et al, 2010b). This power of prediction might allow doctors to diagnose neurodegenerative disorders like PD or AD earlier (Džoljić et al, 2005). In addition, other data have shown the potential role of GABAergic striatal interneurons expressing somatostatin, neuropeptide Y, NADPH diaphorase and NOS in compensation for dopamine loss in experimental or idiopathic PD (Ibáñez-Sandoval et al, 2010).…”

Section: Neurotoxicitymentioning

confidence: 99%

“…The results of various studies have shown that in the central nervous system (CNS) NO expresses not only cytoprotective but also cytotoxic effects (Boje, 2004;Akyol et al, 2004;Colasanti and Suzuki, 2000). The list of pathological conditions in which NO has been shown to be an important mediator is increasing and alterations of the NO system could be implicated in a wide variety of neurological diseases (Colasanti and Suzuki, 2000;Džoljić et al, 2005;Nakamura et al, 2010a). NO was proclaimed "Molecule of the Year" for 1992 by the journal Science, and six years later the Nobel Prize in Physiology or Medicine was awarded to scientists who had discovered NO pathways and shed light on the roles of NO (Zhou et al, 2009) ) (Tieu et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…However, these new findings reveal that NO can actually be transferred from one protein to another in molecular pathways that lead to cellular suicide. This fact can be used to better diagnose and treat diseases like Parkinson's, Huntington's or Alzheimer's disease (Džoljić et al, 2005;Nakamura and Lipton, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Why is nitric oxide important for our brain?

Džoljić¹,

Grbatinić²,

Kostić³

2015

Functional Neurology

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SummaryThe freely diffusible gaseous compound nitric oxide (NO) has been shown to be an important messenger in many organ systems throughout the body, and particularly in the central nervous system (CNS). The importance of NO as an intermediary in cell communication in the brain is highlighted by the fact that the excitatory amino acid glutamate, the most abundant CNS neurotransmitter, is an initiator of the reaction that forms NO. Because of its numerous physiological and pathophysiological roles, the impact of NO on clinical medicine is developing. NO can act as a "double-edged sword" and it has been demonstrated that clarification of the dual effect of NO might have implications for clinical medicine, and could lead to the emergence of therapeutic opportunities. Accordingly, NO was proclaimed "Mole cule of the Year" in 1992 by the journal Science, while discovery of the pathways and roles of NO was acknowledged with the Nobel Prize in 1998. Additionally, the ubiquity of NO in the CNS implies that drugs designed to modify the biological activity of NO may have distinct effects. Thus, further clinical applications of NO, of its analogs or of newly developed NOS inhibitors are forthcoming. The therapeutic challenge would be to succeed in manipulating the NO pathways selectively.

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Section: Neurodegenerationmentioning

confidence: 71%

Section: Neurodegenerationmentioning

confidence: 99%

Section: Neurotoxicitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Why is nitric oxide important for our brain?

Džoljić¹,

Grbatinić²,

Kostić³

2015

Functional Neurology

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Catalpol protects against 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells

Choi

Suh

Jung

et al. 2019

J of Applied Toxicology

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2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) is a well‐known environmental contaminant that produces a wide variety of adverse effects in humans. Catalpol, a major bioactive compound enriched in the dried root of Rehmannia glutinosa, is a major iridoid glycoside that alleviates bone loss. However, the detailed mechanisms underlying the effects of catalpol remain unclear. The present study evaluated the effects of catalpol on TCDD‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells. Catalpol inhibited TCDD‐induced reduction in cell viability and increases in apoptosis and autophagic activity in osteoblastic MC3T3‐E1 cells. Additionally, pretreatment with catalpol significantly decreased the nitric oxide and nitrite levels compared with a control in TCDD‐treated cells and significantly inhibited TCDD‐induced increases in the levels of cytochrome P450 1A1 and extracellular signal‐regulated kinase. Pretreatment with catalpol also effectively restored the expression of superoxide dismutase and extracellular signal‐regulated kinase 1 and significantly enhanced the expression of glutathione peroxidase 4 and osteoblast differentiation markers, including alkaline phosphatase and osterix. Taken together, these findings demonstrate that catalpol has preventive effects against TCDD‐induced damage in MC3T3‐E1 osteoblastic cells.

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Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

Matteo

Pierucci

Esposito

et al. 2008

Progress in Brain Research

138

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Several recent studies have emphasized a crucial role for the interactions between serotonergic and dopaminergic systems in movement control and the pathophysiology of basal ganglia. These observations are supported by anatomical evidence demonstrating large serotonergic innervation of all the basal ganglia nuclei. In fact, serotonergic terminals have been reported to make synaptic contacts with both substantia nigra dopamine-containing neurons and their terminal areas such as the striatum, the globus pallidus and the subthalamus. These brain areas contain a high concentration of serotonin (5-HT), with the substantia nigra pars reticulata receiving the greatest input. In this chapter, the distribution of different 5-HT receptor subtypes in the basal ganglia nuclei will be described. Furthermore, evidence demonstrating the serotonergic control of basal ganglia activity will be reviewed and the contribution of the different 5-HT receptor subtypes examined. The new avenues that the increasing knowledge of 5-HT in motor control has opened for exploring the pathophysiology and pharmacology of Parkinson's disease and other movement disorders will be discussed. It is clear that these avenues will be fruitful, despite the disappointing results so far obtained by clinical studies with selective 5-HT ligands. Nevertheless, these studies have led to a great increase in the attention given to the neurotransmitters of the basal ganglia and their connections.

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Azotni oksid, neurodegeneracija i Parkinsonova bolest

Cited by 4 publications

References 64 publications

Why is nitric oxide important for our brain?

Why is nitric oxide important for our brain?

Catalpol protects against 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells

Serotonin modulation of the basal ganglia circuitry: therapeutic implication for Parkinson's disease and other motor disorders

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