2018
DOI: 10.1080/14767058.2017.1419175
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Caffeine prevents bilirubin-induced cytotoxicity in cultured newborn rat astrocytes

Abstract: Caffeine seems encouraging for the prevention and treatment of bilirubin neurotoxicity in rats by means of its antiapoptotic, antioxidant, anti-inflammatory, anti-nitrosative, and anti-TLR-4 properties.

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Cited by 15 publications
(8 citation statements)
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“…These models can be used to study the effect of therapeutic interventions such as caffeine, which are not completely understood [29][30][31]. In addition to antagonism of adenosine receptors [32], anti-inflammatory effects, and the reduction of stress on the endoplasmic reticulum, anti-oxidant properties per se have also been discussed [33][34][35][36]. Therefore, this study aims to investigate the action of caffeine on the oxidative stress response in pulmonary tissue in a hyperoxia-based model of BPD in the newborn rat.…”
Section: Introductionmentioning
confidence: 99%
“…These models can be used to study the effect of therapeutic interventions such as caffeine, which are not completely understood [29][30][31]. In addition to antagonism of adenosine receptors [32], anti-inflammatory effects, and the reduction of stress on the endoplasmic reticulum, anti-oxidant properties per se have also been discussed [33][34][35][36]. Therefore, this study aims to investigate the action of caffeine on the oxidative stress response in pulmonary tissue in a hyperoxia-based model of BPD in the newborn rat.…”
Section: Introductionmentioning
confidence: 99%
“…This scenario underscores the importance of the altered function of different compartments to understand how the intake of caffeine predisposes the brain to better handle noxious stimuli. In fact, apart from the metabolic adaptation of cortical synapses, astrocytes also emerge as a putative target to be modified by caffeine, as hinted by previous observations (e.g., [79,80]) but still awaiting a direct demonstration. In this respect, it is important to keep in mind that the neuroprotection afforded by caffeine might also involve additional cell types such as microglia orchestrating neuroinflammation and neuro-vascular coupling that also contribute to the outcome of brain damage (reviewed in [81,82]) and that are controlled by caffeine [69,83].…”
Section: Discussionmentioning
confidence: 79%
“…The mechanism of unconjugated bilirubin-induced neuron damage has not been fully elucidated. Existing hypotheses include excitotoxicity hypotheses ( 17 ), bilirubin-induced neuroinflammation ( 18 , 19 ), and oxidative stress mechanisms ( 20 ). The destruction of bilirubin on neurons is recoverable in the early stages; consequently, early identification of ABE risk factors and intervention is an important method to prevent ABE, reduce the sequelae, and improve the prognosis.…”
Section: Discussionmentioning
confidence: 99%