A new rat model of neonatal bilirubin encephalopathy (kernicterus)

Amini, Naser; Vousooghi, Nasim; Soleimani, Mansoureh; Samadikuchaksaraei, Alí; Akbari, Mehdi; Safakheil, Hosein; Atafimanesh, Pezhman; Shahbazi, Ali; Milan, Peiman Brouki; Ramezani, Sara; Mozafari, Masoud; Joghataei, Mohammad Taghi

doi:10.1016/j.vascn.2016.10.002

Cited by 16 publications

(6 citation statements)

References 27 publications

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“…Coupled with the apparent sparing of the hair cells, this model warrants further investigation as a potential candidate for neural progenitor transplant. As might be expected, the PHZ-induced damage can be exacerbated by co-injection with sulfa (Amini et al, 2017).…”

Section: Neonatal Jaundicesupporting

confidence: 58%

The use of animal models to study cell transplantation in neuropathic hearing loss

Abbas

Rivolta

2019

Hearing Research

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Auditory neuropathy (AN) is a form of sensorineural deafness specifically affecting the conduction of the nerve impulse from the cochlear hair cells to the auditory centres of the brain. As such, the condition is a potential clinical target for 'cell replacement therapy', in which a functioning auditory nerve is regenerated by transplanting an appropriated neural progenitor. In this review, we survey the current literature and examine possible experimental models for this condition, with particular reference to their compatibility as suitable hosts for transplantation. The use of exogenous neurotoxic agents such as ouabain or β-bungarotoxin is discussed, as are ageing and noise-induced synaptopathy models. Lesioning of the nerve by mechanical damage during surgery and the neuropathy resulting from infectious diseases may be very relevant clinically, and we discuss whether there are good models for these situations. We also address genetic models for AN, examining whether the phenotypes truly model the clinical situation in their human counterpart syndromes-we use the example of the hyperbilirubinaemic Gunn rat as a particular instance in this regard.

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Section: Neonatal Jaundicesupporting

confidence: 58%

The use of animal models to study cell transplantation in neuropathic hearing loss

Abbas

Rivolta

2019

Hearing Research

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“…The same treatment induces brain damage also in wild type Wistar rats [ 14 ]. Recently combined administration of phenylhydrazine and sulfisoxazole to produce hypo-albuminemia was described for the induction of kernicterus in Wistar rats [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Monitoring the Response of Hyperbilirubinemia in the Mouse Brain by In Vivo Bioluminescence Imaging

Manni¹,

Rocco²,

Fusco

et al. 2016

IJMS

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Increased levels of unconjugated bilirubin are neurotoxic, but the mechanism leading to neurological damage has not been completely elucidated. Innovative strategies of investigation are needed to more precisely define this pathological process. By longitudinal in vivo bioluminescence imaging, we noninvasively visualized the brain response to hyperbilirubinemia in the MITO-Luc mouse, in which light emission is restricted to the regions of active cell proliferation. We assessed that acute hyperbilirubinemia promotes bioluminescence in the brain region, indicating an increment in the cell proliferation rate. Immunohistochemical detection in brain sections of cells positive for both luciferase and the microglial marker allograft inflammatory factor 1 suggests proliferation of microglial cells. In addition, we demonstrated that brain induction of bioluminescence was altered by pharmacological displacement of bilirubin from its albumin binding sites and by modulation of the blood–brain barrier permeability, all pivotal factors in the development of bilirubin-induced neurologic dysfunction. We also determined that treatment with minocycline, an antibiotic with anti-inflammatory and neuroprotective properties, or administration of bevacizumab, an anti-vascular endothelial growth factor antibody, blunts bilirubin-induced bioluminescence. Overall the study supports the use of the MITO-Luc mouse as a valuable tool for the rapid response monitoring of drugs aiming at preventing acute bilirubin-induced neurological dysfunction.

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“…Bilirubin encephalopathy is a serious complication of neonatal jaundice [ 7 ]. High concentrations of UCB in the blood can easily cross the blood-brain barrier and damage neurons, resulting in neurological disability or even death [ 15 ]. Although the mechanism of neurotoxicity induced by UCB is not well understood, previous research indicates that oxidative stress and apoptosis may play a role in damaging neurons [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

Song

2018

Med Sci Monit

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BackgroundBilirubin encephalopathy is a serious complication in neonatal jaundice and is associated with high mortality and disability in newborns. The present study aimed to investigate the neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) on bilirubin encephalopathy in vitro and in vivo.Material/MethodsThe cytotoxicity of unconjugated bilirubin (UCB) to neurons and neuroprotection of ω-3 PUFA were investigated using MTT assays and apoptosis evaluations. Superoxide dismutase (SOD) and catalase (CAT) enzyme activity were measured to investigate the anti-oxidative effect of ω-3 PUFA. The differences between eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were also compared. The in vivo neuroprotective effect of DHA was demonstrated in neonatal rats with bilirubin encephalopathy by bilirubin monitoring, neuron-specific enolase (NSE) monitoring, H&E staining of brain tissue, and apoptosis rate evaluations.ResultsOmega-3 PUFA reduced the rate of apoptosis induced by UCB and increased SOD and CAT enzyme activity for anti-oxidation. DHA did not reduce the bilirubin in the serum of neonatal rats with bilirubin encephalopathy, but did reduce the damage caused by bilirubin with decreased NSE and apoptosis rate as well as improved neuron morphology.ConclusionsOmega-3 PUFA, particularly DHA, can reduce neurological damage in neonatal rats with bilirubin encephalopathy by increasing anti-apoptosis and anti-oxidation effects against UCB, providing a theoretical basis for the clinical treatment of bilirubin encephalopathy in newborns.

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A new rat model of neonatal bilirubin encephalopathy (kernicterus)

Cited by 16 publications

References 27 publications

The use of animal models to study cell transplantation in neuropathic hearing loss

The use of animal models to study cell transplantation in neuropathic hearing loss

Monitoring the Response of Hyperbilirubinemia in the Mouse Brain by In Vivo Bioluminescence Imaging

Neuroprotective Effect of ω-3 Polyunsaturated Fatty Acids on Bilirubin Encephalopathy In Vitro and In Vivo

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