Drug delivery platforms for neonatal brain injury

Narayanamurthy, Rukhmani; Yang, Jung‐Lynn Jonathan; Yager, Jerome Y.; Unsworth, Larry D.

doi:10.1016/j.jconrel.2020.12.056

Cited by 10 publications

(4 citation statements)

References 324 publications

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“…HIE is a common neonatal disease in clinical practice at present, and the pathogenesis includes mitochondrial damage, oxidative stress, neurotoxicity of excitatory amino acids, and in ammatory immune response due to the results of a combination of cellular and molecular mechanisms. Its occurrence is mainly related to perinatal asphyxia and plays an indispensable role in perinatal neurological diseases, which can cause brain tissue hypoxia, interruption or reduction of cerebral blood ow, brain injury in newborns, neurological injury, and severe death in children (Schump, 2018;Narayanamurthy et al, 2021).There is increasing evidence that HI causes irreversible brain damage to the developing brain, leading to long-term neurological de cits. The incidence of neurological sequelae is relatively high, resulting in an increased incidence of disability, and the earlier this type of disease, the better the therapeutic effect.…”

Section: Discussionmentioning

confidence: 99%

“…HIE is a common neonatal disease in clinical practice at present, and the pathogenesis includes mitochondrial damage, oxidative stress, neurotoxicity of excitatory amino acids, and inflammatory immune response due to a combination of cellular and molecular mechanisms. Its occurrence is mainly related to perinatal asphyxia and plays an indispensable role in perinatal neurological diseases, which can cause brain tissue hypoxia, interruption or reduction of cerebral blood flow, brain injury in newborns, neurological injury, and even death in children 50,51 . At present, mild hypothermia therapy is often used to treat moderate and severe full‐term HIE children in clinical practice, which has a regulatory effect on the body's cerebral blood flow and can reduce neuronal apoptosis and relieve neurological symptoms such as disturbance of consciousness and floppy limbs in children 52 .…”

Section: Discussionmentioning

confidence: 99%

“…Its occurrence is mainly related to perinatal asphyxia and plays an indispensable role in perinatal neurological diseases, which can cause brain tissue hypoxia, interruption or reduction of cerebral blood flow, brain injury in newborns, neurological injury, and even death in children. 50 , 51 At present, mild hypothermia therapy is often used to treat moderate and severe full‐term HIE children in clinical practice, which has a regulatory effect on the body's cerebral blood flow and can reduce neuronal apoptosis and relieve neurological symptoms such as disturbance of consciousness and floppy limbs in children. 52 It is undeniable that hypothermia treatment is recognized as an effective treatment for HIE.…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Fei‐Sun

Huang

Qin

et al. 2022

Ibrain

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Hypoxic ischemic encephalopathy (HIE) is an important cause of neonatal death and disability, which can lead to long-term neurological and motor dysfunction. At present, the treatment mainly focuses on the symptomatic treatment in the acute phase and rehabilitation after injury, but the effect is not satisfactory, and more effective methods are urgently needed. Due to the widespread use of inhalation anesthetics in surgery, it has been found that iso urane (ISO) preconditioning may have a positive effect on neuroprotection. The aim of this study was to investigate the effects of ISO preconditioning on neurological function and behavior in HIE rats. MethodsNeonatal rats were used to create hypoxic-ischemic (HI) model by ligating the right common carotid artery at 7 days and then in a hypoxia chamber. The effects of anesthetic drugs on neurological function after one hour of ISO preconditioning were assessed after modeling by Morris water maze(MWM), Ymaze, and rotarod tests at one month. Thereafter, samples were taken at 1 and 42 days for Nissl staining and Hematoxylin-Eosin (HE) staining to observe neuronal number and histomorphology changes. The relationship of behaviour and morphology tests were measured. ResultsIschemia and hypoxia could induce neuronal injury, neurological dysfunction and severe long-term motor function injury. Histological staining and behavioural evaluations were performed to elucidate the pathological changes and neurobehavioural variation after ISO treatment. We found ISO administration signi cantly reduced the infarct volume of brain tissues and improved the autonomous activities of neonatal rats, ISO preconditioning signi cantly reduced neuronal apoptosis induced by HI, reduced cerebral infarction volume, improved histopathological damage of nerve cells, improved long-term cognitive function, and attenuated HI-induced Nissl total cells to reduce and reduce long-term spatial memory impairment caused by hypoxia-ischemia during the maturation of injured brain. ConclusionISO preconditioning can protect the brain injury and promote the recovery of neurological function in neonatal rats with HIE, which may be through inhibiting the neuronal cell death in the cortex and hippocampus after HI.

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Section: Discussionmentioning

confidence: 99%

“…HIE is a common neonatal disease in clinical practice at present, and the pathogenesis includes mitochondrial damage, oxidative stress, neurotoxicity of excitatory amino acids, and inflammatory immune response due to a combination of cellular and molecular mechanisms. Its occurrence is mainly related to perinatal asphyxia and plays an indispensable role in perinatal neurological diseases, which can cause brain tissue hypoxia, interruption or reduction of cerebral blood flow, brain injury in newborns, neurological injury, and even death in children 50,51 . At present, mild hypothermia therapy is often used to treat moderate and severe full‐term HIE children in clinical practice, which has a regulatory effect on the body's cerebral blood flow and can reduce neuronal apoptosis and relieve neurological symptoms such as disturbance of consciousness and floppy limbs in children 52 .…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Fei‐Sun

Huang

Qin

et al. 2022

Ibrain

View full text Add to dashboard Cite

show abstract

“…Neonatal hypoxic‐ischemic brain damage (HIBD), also referred to as neonatal hypoxic‐ischemic encephalopathy (HIE), is a leading cause of infant mortality and irreversible long‐term neurodevelopmental impairments (Schreglmann et al, 2020 ). HIE‐related complications account for approximately 23% of infant deaths worldwide, impacting 700,000–1,200,000 newborns annually (Lawn et al, 2005 ; Narayanamurthy et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Protective mechanisms of quercetin in neonatal rat brain injury induced by hypoxic‐ischemic brain damage (HIBD)

Xu,

Chen

et al. 2023

Food Science & Nutrition

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Neonatal hypoxic‐ischemic brain damage (HIBD) is a leading cause of infant mortality worldwide. This study explored whether quercetin (Que) exerts neuroprotective effects in a rat model of HIBD. A total of 36 seven‐day‐old Sprague–Dawley rats were divided into control, Que, HI, and HI + Que groups. The Rice method was used to establish HIBD in HI and HI + Que rats, which were treated with hypoxia (oxygen concentration of 8%) for 2 h after ligation of the left common carotid artery. The rats in the HI + Que group were intraperitoneally injected with Que (30 mg/kg) 1 h before hypoxia, and the rats in the Que group were only injected with the same amount of Que. Brain tissues were harvested 24 h postoperation and assessed by hematoxylin and eosin staining, 2,3,5‐triphenyltetrazolium chloride staining, and terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay; relative gene and protein levels were evaluated by RT‐qPCR, IHC, or western blot (WB) assay. Brain tissue morphologies were characterized by transmission electron microscopy (TEM); LC3B protein levels were assessed by immunofluorescence staining. Escape latencies and platform crossing times were significantly improved (p < .05) in HI + Que groups; infarct volume significantly decreased (p < .001), whereas the numbers of autophagic bodies and apoptotic cells increased and decreased, respectively. Meanwhile, NLRX1, ATG7, and Beclin1 expressions were significantly upregulated, and mTOR and TIM23 expressions, LC3B protein level, and LC 3II/LC 3I ratio were significantly downregulated. Que exerted neuroprotective effects in a rat model of HIBD by regulating NLRX1 and autophagy.

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