Brain cooling reduces the risk of postneonatal epilepsy in newborns affected by moderate to severe hypoxic-ischemic encephalopathy

Lugli, Licia; Balestri, Eleonora; Berardi, Alberto; Guidotti, Isotta; Cavalleri, Francesca; Todeschini, Alice; Pugliese, Marisa; Casa, Elisa Muttini Della; Lucaccioni, Laura; Ferrari, Fabrizio

doi:10.23736/s2724-5276.18.05224-6

Cited by 9 publications

(9 citation statements)

References 26 publications

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“…Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway clinically available treatment method for HIE, only 50% of treatments are effective (3,5), and there is an urgent need to develop novel treatment approaches.…”

Section: Original Articlementioning

confidence: 99%

“…Neonatal hypoxic-ischemic encephalopathy (HIE) is a type of newborn brain damage caused by cerebral hypoxic ischemia, which is one of the main causes of neonatal death and disability worldwide (1). Surviving children with HIE often have neurological sequelae, such as epilepsy, mental retardation, and cerebral palsy, which can seriously affect their quality of life (2)(3)(4). While hypothermia is the only…”

Section: Introductionmentioning

confidence: 99%

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Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

Cai¹,

Li²,

Tan³

et al. 2022

Transl Pediatr

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Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of neonatal death, and vitamin D (VD) is a neuroprotection nutrition whose deficiency is associated with its risk. However, the mechanism of VD involved in neonatal HIE is not well known. Methods:In this experiment a hypoxic-ischemic brain damage (HIBD) model was established by using the Rice-Vannucci method, rats were intraperitoneally injected with 0.1 μg/kg VD every day for two weeks. The brain damage and mitochondria injury were examined by hematoxylin-eosin (HE) staining and transmission electron microscope (TEM), respectively. The oxidation response and inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA), and the cell viability was determined by Cell Counting Kit-8 (CCK-8). mRNA and protein expression were detected by quantitative real real-time PCR (qRT-PCR), Western blot, and immunofluorescence. Results:The results showed VD effectively ameliorated brain histologic damage and mitochondria injury induced by hypoxic ischemia (HI). VD elevated the expression of Nrf2 and HO-1, which resulted in increased levels of GPX4, superoxide dismutase (SOD), and glutathione (GSH) and reduced content of malondialdehyde (MDA) and reactive oxygen species (ROS), resulting in decreased ferroptosis in HItreated rats. Moreover, VD reduced the secretion of inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β.Conclusions: VD suppresses ferroptosis through activation of the Nrf2/HO-1 signaling pathway and exerts a protective role in neonatal HIE.

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Section: Original Articlementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

Cai¹,

Li²,

Tan³

et al. 2022

Transl Pediatr

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“…p-EEG signals at 24, 48, and 72 h were classified according to the system described by Murray et al [ 14 ]. A seizure was defined as a sudden, repetitive, stereotyped discharge lasting ≥10 s on two or more EEG channels [ 21 , 22 ] ( Figure 1 ). Antiepileptic drugs (AEDs) were administered based on online p-EEG evaluations.…”

Section: Methodsmentioning

confidence: 99%

“…Antiepileptic drugs (AEDs) were administered based on online p-EEG evaluations. According to the local protocol, phenytoin was administered as the first-line and midazolam as the second-line AED [ 21 , 22 ].…”

Section: Methodsmentioning

confidence: 99%

“…Neurodevelopmental outcomes were classified as normal (absent neurological signs and DQ > 85), moderately abnormal (clumsiness, poor balance, DQ 70–85, hearing impairment with no amplification), or severely abnormal (cerebral palsy, DQ < 70, epilepsy, a severe sensorineural deficit like bilateral deafness, requiring bilateral hearing aids or unilateral or bilateral cochlear implants, or bilateral blindness with visual acuity < 6/60 in the better eye) [ 21 , 22 ]. Cerebral palsy (CP) was defined as spastic (diplegia, hemiplegia, or quadriplegia), dystonic, or athetoid [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

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Polygraphic EEG Can Identify Asphyxiated Infants for Therapeutic Hypothermia and Predict Neurodevelopmental Outcomes

et al. 2022

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Background: Neonatal encephalopathy due to perinatal asphyxia is one of the leading causes of neonatal death and morbidity worldwide. The neurodevelopmental outcomes of asphyxiated neonates have considerably improved after therapeutic hypothermia (TH). The current challenge is to identify all newborns with encephalopathy at risk of cerebral lesions and subsequent disability within 6 h of life and who may be within the window period for treatment with TH. This study evaluated the neurodevelopmental outcomes in surviving asphyxiated neonates who did and did not receive TH, based on clinical and polygraphic electroencephalographic (p-EEG) criteria. Methods: The study included 139 asphyxiated newborns divided into two groups: 82 who received TH and 57 who were not cooled. TH was administered to asphyxiated newborns (gestational age ≥ 35 weeks, birth weight ≥ 1800 g) with encephalopathy of any grade and moderate-to-severe p-EEG abnormalities or seizures. Neurodevelopmental outcomes between the groups at 24 months of life and the risk factors for severe outcomes were assessed. Results: Severe neurodevelopmental impairment occurred in 10 (7.2%) out of the 139 enrolled neonates. Nine out of the 82 cooled neonates (11.0%) had severe neurodevelopmental impairment. All but one neonate (98.2%) who did not receive TH had normal outcomes. The multivariate logistic regression analysis showed that abnormal p-EEG patterns (OR: 27.6; IC: 2.8–267.6) and general movements (OR: 3.2; IC: 1.0–10.0) were significantly associated with severe neurodevelopmental impairment (area under ROC curve: 92.7%). Conclusion: The combination of clinical and p-EEG evaluations in hypoxic–ischemic encephalopathy contributed to a more accurate selection of patients treated with therapeutic hypothermia. When administered to infants with moderate to severe p-EEG abnormalities, TH prevents approximately 90% of severe neurodevelopmental impairment after any grade of hypoxic–ischemic encephalopathy.

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Ghrelin attenuates oxidative stress and neuronal apoptosis via GHSR-1α/AMPK/Sirt1/PGC-1α/UCP2 pathway in a rat model of neonatal HIE

Huang

Liu

Doycheva

et al. 2019

Free Radical Biology and Medicine

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Brain cooling reduces the risk of postneonatal epilepsy in newborns affected by moderate to severe hypoxic-ischemic encephalopathy

Cited by 9 publications

References 26 publications

Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

Polygraphic EEG Can Identify Asphyxiated Infants for Therapeutic Hypothermia and Predict Neurodevelopmental Outcomes

Ghrelin attenuates oxidative stress and neuronal apoptosis via GHSR-1α/AMPK/Sirt1/PGC-1α/UCP2 pathway in a rat model of neonatal HIE

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