Research progress of neonatal hypoxic‐ischemic encephalopathy in nonhuman primate models

Guan, Yi‐Huan; Zhou, Huijie; Luo, Bo‐Yan; Hussain, Sajid; Xiong, Liu‐Lin

doi:10.1002/ibra.12097

Cited by 4 publications

(1 citation statement)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, severe surgical trauma and long recovery time restrict the use of pregnant sheep as a model for HIE studies. Non-human primates are believed to be the most ideal and appropriate animal models for HIE studies because they are the most evolved and closest to humans, such as the macaques (Kobayashi et al, 2018;Guan et al, 2023). The acute perinatal asphyxia model has been successfully established in non-human primates using umbilical cord obstruction (UCO) to induce moderate to severe HIE before delivery (Traudt et al, 2013;McAdams et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities

She,

Sun,

Chen

et al. 2023

Front. Neurosci.

View full text Add to dashboard Cite

Hypoxic-ischemic encephalopathy (HIE) is the leading cause of long-term neurological disability in neonates and adults. Through bibliometric analysis, we analyzed the current research on HIE in various countries, institutions, and authors. At the same time, we extensively summarized the animal HIE models and modeling methods. There are various opinions on the neuroprotective treatment of HIE, and the main therapy in clinical is therapeutic hypothermia, although its efficacy remains to be investigated. Therefore, in this study, we discussed the progress of neural circuits, injured brain tissue, and neural circuits-related technologies, providing new ideas for the treatment and prognosis management of HIE with the combination of neuroendocrine and neuroprotection.

show abstract

Section: Introductionmentioning

confidence: 99%

Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities

She,

Sun,

Chen

et al. 2023

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

Tibetan-Origin Edible Chinese Herbal Prescription C18 Protects H9C2 Cardiomyocytes from Cobalt Chloride-induced Hypoxia Injury through the PI3K/AKT Signaling Pathway

Chang,

Xie,

Chen

et al. 2024

Pharmacognosy Magazine

View full text Add to dashboard Cite

Background Altitude sickness is often prone to occur during tourism or work in high-altitude areas. In China, traditional Tibetan medicines have a long history of preventing or treating altitude sickness, especially altitude hypoxia, which may lead to myocardial cell apoptosis and myocardial hypoxia-reoxygenation injury. Purpose This study investigated the effect of a Tibetan-origin edible Chinese herbal prescription (named C18) on protecting H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury and its potential mechanism. Methods In this study, a hypoxic injury model of H9C2 cardiomyocytes induced by cobalt chloride was established first. Then the cell viability, relevant antioxidant indicators malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and protein expression (hypoxia-inducible factor 1 alpha (HIF-1α), phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT)) were measured after pretreatment with or without C18. At last, the specific PI3K/AKT inhibitor LY294002 was applied to verify the antihypoxia signaling pathway. Results C18 could significantly promote normal H9C2 cardiomyocyte proliferation and inhibit apoptosis of hypoxic H9C2 cardiomyocytes, reduce the release of lactate dehydrogenase and MDA, and increase the levels of SOD and GSH-Px antioxidant enzymes. In addition, C18 could significantly downregulate the expression of HIF-1α protein and upregulate the expression of intracellular p-AKT. Moreover, these effects of C18 can be blocked by the specific PI3K/AKT inhibitor LY294002. Conclusion C18 protects H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury through the PI3K/AKT signaling pathway.

show abstract

The Importance of Including Maternal Immune Activation in Animal Models of Hypoxic–Ischemic Encephalopathy

Collins,

Lemanski,

Wright-Jin

2024

Biomedicines

View full text Add to dashboard Cite

Hypoxic–ischemic encephalopathy (HIE) is a perinatal brain injury that is the leading cause of cerebral palsy, developmental delay, and poor cognitive outcomes in children born at term, occurring in about 1.5 out of 1000 births. The only proven therapy for HIE is therapeutic hypothermia. However, despite this treatment, many children ultimately suffer disability, brain injury, and even death. Barriers to implementation including late diagnosis and lack of resources also lead to poorer outcomes. This demonstrates a critical need for additional treatments for HIE, and to facilitate this, we need translational models that accurately reflect risk factors and interactions present in HIE. Maternal or amniotic infection is a significant risk factor and possible cause of HIE in humans. Maternal immune activation (MIA) is a well-established model of maternal infection and inflammation that has significant developmental consequences largely characterized within the context of neurodevelopmental disorders such as autism spectrum disorder and schizophrenia. MIA can also lead to long-lasting changes within the neuroimmune system, which lead to compounding negative outcomes following a second insult. This supports the importance of understanding the interaction of maternal inflammation and hypoxic–ischemic outcomes. Animal models have been invaluable to understanding the pathophysiology of this injury and to the development of therapeutic hypothermia. However, each model system has its own limitations. Large animal models such as pigs may more accurately represent the brain and organ development and complexity in humans, while rodent models are more cost-effective and offer more possible molecular techniques. Recent studies have utilized MIA or direct inflammation prior to HIE insult. Investigators should thoughtfully consider the risk factors they wish to include in their HIE animal models. In the incorporation of MIA, investigators should consider the type, timing, and dose of the inflammatory stimulus, as well as the timing, severity, and type of hypoxic insult. Using a variety of animal models that incorporate the maternal–placental–fetal system of inflammation will most likely lead to a more robust understanding of the mechanisms of this injury that can guide future clinical decisions and therapies.

show abstract

Research progress of neonatal hypoxic‐ischemic encephalopathy in nonhuman primate models

Cited by 4 publications

References 65 publications

Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities

Current analysis of hypoxic-ischemic encephalopathy research issues and future treatment modalities

Tibetan-Origin Edible Chinese Herbal Prescription C18 Protects H9C2 Cardiomyocytes from Cobalt Chloride-induced Hypoxia Injury through the PI3K/AKT Signaling Pathway

The Importance of Including Maternal Immune Activation in Animal Models of Hypoxic–Ischemic Encephalopathy

Contact Info

Product

Resources

About