Effect of mouse nerve growth factor on the expression of glial fibrillary acidic protein in hippocampus of neonatal rats with hypoxic-ischemic brain damage

Yin, Xiaoxing; Lei, Dong; Wei, Wei; Wang, Yu; Chai, Yannan; Feng, Zhichun

doi:10.3892/etm.2012.827

Cited by 5 publications

(4 citation statements)

References 12 publications

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“…4,5 The prevalence of HIBD is about 6 in 1000 survival births, and approximately 25% to 30% of survivals suffer from long-term sequela, and thus it is a major cause reducing the quality of life of children across the world. 6 Following neonatal HIBD, changes of synaptic functions and electrophysiological characteristics instantly occur in the hippocampal CA1 pyramidal cells. 7,8 The neurological impairments due to HIBD include cerebral palsy, epilepsy, mental retardation, or even psychiatric problems, and the patients commonly suffer from a lifelong disability and a higher susceptibility to epilepsy, occurring in 15% to 60% of the children with cerebral palsy.…”

Section: Introductionmentioning

confidence: 99%

“…Neonatal HIBD represents the brain injuries induced by the hypoxia‐ischemia (HI) following perinatal suffocation, including a temporary occlusion or a reduction of cerebral blood flow, and has the characteristics of abnormalities in the central nervous system (CNS) . The prevalence of HIBD is about 6 in 1000 survival births, and approximately 25% to 30% of survivals suffer from long‐term sequela, and thus it is a major cause reducing the quality of life of children across the world . Following neonatal HIBD, changes of synaptic functions and electrophysiological characteristics instantly occur in the hippocampal CA1 pyramidal cells .…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of the PI3K/Akt signaling pathway impedes the restoration of neurological function following hypoxic‐ischemic brain damage in a neonatal rabbit model

Luo

Zhang

Niu

et al. 2019

J of Cellular Biochemistry

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Objective: Hypoxic-ischemic brain damage (HIBD), frequently occurring in infancy and childhood, is a major cause of mortality and severe neurologic impairment. This study was performed to examine the effect of the PI3K/Akt signaling pathway on HIBD in a neonatal rabbit model. Materials and Methods:Uterine artery occlusion was used to establish HIBD models in neonatal rabbits, which were then subjected to sham operation, dimethyl sulfoxide (2 mL) or LY294002 (inhibitor of PI3K/Akt signaling pathway, 6.4 μg/kg).Behavioral neurological assessment was performed in neonatal rabbits delivered by cesarean section, after which serum neuron-specific enolase (NSE) level and cerebral water content were determined. The level of cleaved caspase-3 level and apoptosis of neurons were observed by immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining.Furthermore, the expression of PI3K/Akt signaling pathway-and apoptosis-related factors was examined.Results: In neonatal rabbits, HIBD increased the fetal death rate; reduced neurological scores of posture, righting reflex, and deglutition reflex; elevated serum NSE levels, cerebral water content, cleaved caspase-3-positive expression in hippocampal CA1 region and apoptotic neurons; inactivated PI3K/Akt signaling pathway as well as reduced Bcl-2 expression and increased BAD and Bax expression. Notably, the treatment of LY294002 further aggravated neurological impairment in neonatal rabbits in response to HIBD.Conclusion: Following the HIBD caused by intrauterine asphyxia, the LY294002 administered through auricular vein infusion into pregnant rabbits exacerbates neurological impairment of neonatal rabbits, suggesting that inhibition of PI3K/ Akt signaling pathway may serve as a candidate therapeutic target for neurological recovery. K E Y W O R D Sapoptosis, caspase-3, hypoxic-ischemic brain damage, LY294002, neonatal rabbit, neurological impairment, neuron, PI3K/Akt signaling pathway

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of the PI3K/Akt signaling pathway impedes the restoration of neurological function following hypoxic‐ischemic brain damage in a neonatal rabbit model

Luo

Zhang

Niu

et al. 2019

J of Cellular Biochemistry

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“…In children with CP, the addition of acupuncture injections of mNGF to the rehabilitation treatment can more effectively reduce blood lactate levels and improve motor function [20]. A study by Yin et al found that the mNGF treatment at a dose of 20 ng/g/day significantly promoted hippocampal neurogenesis and inhibited neuronal apoptosis in newborn rats with hypoxic-ischemic brain injury [21]; however, whether mNGF suppresses neuronal apoptosis and alleviates ASD remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Mouse nerve growth factor suppresses neuronal apoptosis in valproic acid-induced autism spectrum disorder rats by regulating the phosphoinositide-3-kinase/serine/threonine kinase signaling pathway

Jian

Zhao

et al. 2023

Pharmacogenetics and Genomics

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Background Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and restrictive behaviors. Mouse nerve growth factor (mNGF), a neurotrophic factor, is critical for neuronal growth and survival, and the mNGF treatment is considered a promising therapy for neurodegeneration. In light of this, we aimed to evaluate the effect of mNGF on neurological function in ASD.Methods An ASD rat model was established by intraperitoneal injection of valproic acid (VPA). Social behavior, learning, and memory of the rats were measured. TdT-mediated dUTP Nick-end labeling and Nissl assays were performed to detect neuronal apoptosis and survival in the hippocampus and prefrontal cortex. Apoptosisrelated proteins and oxidative stress markers were detected.Results mNGF improved locomotor activity, exploratory behavior, social interaction, and spatial learning and memory in VPA-induced ASD rats. In the hippocampus and prefrontal cortex, mNGF suppressed neuronal apoptosis, increased the number of neurons, superoxide dismutase, and glutathione levels, and decreased reactive oxygen species, nitric oxide, TNF-α, and IL-1β levels compared with the VPA group. In addition, mNGF increased the levels of Bcl-2, p-phosphoinositide-3kinase (PI3K), and p-serine/threonine kinase (Akt), and decreased the levels of Bax and cleaved caspase-3, while the PI3K inhibitor LY294002 reversed these effects. ConclusionThese data suggest that mNGF suppressed neuronal apoptosis and ameliorated the abnormal behaviors in VPA-induced ASD rats, in part, by activating the PI3K/Akt signaling pathway.

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“…Hypoxic-ischemic brain damage (HIBD) in neonates is mainly caused by perinatal asphyxia, and its prevalence is about 1–6% ( 1 ). Nearly one-third of the survivors develop mental retardation, epilepsy, cerebral palsy, and other sequelae ( 2 ). Mild hypothermia is often used to treat HIBD; however, the clinical treatment of HIBD often misses its best therapeutic window and cannot significantly improve the prognosis of children with severe HIBD ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Ferrostatin-1 attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis

Zhang,

Liu,

Zhou

et al. 2023

Transl Pediatr

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Background Hypoxic-ischemic brain damage (HIBD) is a type of brain damage that is caused by perinatal asphyxia and serious damages the central nervous system. At present, there is no effective drug for the treatment of this disease. Besides, the pathogenesis of HIBD remains elusive. While studies have shown that ferroptosis plays an important role in HIBD, its role and mechanism in HIBD are yet to be fully understood. Methods The HIBD model of neonatal rats was established using the Rice-Vannucci method. A complete medium of PC12 cells was adjusted to a low-sugar medium, and the oxygen-glucose deprivation model was established after continuous hypoxia for 12 h. Laser Doppler blood flow imaging was used to detect the blood flow intensity after modeling. 2,3,5-triphenyl tetrazolium chloride staining was employed to detect ischemic cerebral infarction in rat brain tissue, and hematoxylin and eosin staining and transmission electron microscopy were used to observe brain injury and mitochondrial damage. Immunofluorescence was applied to monitor the expression of GFAP. Real-time quantitative polymerase chain reaction, western blot, and immunofluorescence were utilized to detect the expression of messenger RNA and protein. The level of reactive oxygen species (ROS) in cells was detected using the ROS detection kit. Results The results showed that ferrostatin-1 (Fer-1) significantly alleviated the brain injury caused by hypoxia and ischemia. Fer-1 significantly increased the expression of SLC3A2, SLC7A11, ACSL3, GSS, and GPX4 (P<0.05) and dramatically decreased the expressions of GFAP, ACSL4, TFRC, FHC, FLC, 4-HNE, HIF-1α, and ROS (P<0.05). Conclusions Fer-1 inhibits ferroptosis and alleviates HIBD by potentially targeting the GPX4/ACSL3/ACSL4 axis; however, its specific mechanism warrants further exploration.

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Effect of mouse nerve growth factor on the expression of glial fibrillary acidic protein in hippocampus of neonatal rats with hypoxic-ischemic brain damage

Cited by 5 publications

References 12 publications

Inhibition of the PI3K/Akt signaling pathway impedes the restoration of neurological function following hypoxic‐ischemic brain damage in a neonatal rabbit model

Inhibition of the PI3K/Akt signaling pathway impedes the restoration of neurological function following hypoxic‐ischemic brain damage in a neonatal rabbit model

Mouse nerve growth factor suppresses neuronal apoptosis in valproic acid-induced autism spectrum disorder rats by regulating the phosphoinositide-3-kinase/serine/threonine kinase signaling pathway

Ferrostatin-1 attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis

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