Mild hypothermia protects neurons against oxygen glucose deprivation via poly (ADP-ribose) signaling

Gao, Yubo; Wang, Zhihua; He, Weikun; Ma, Wenjing; Ni, Xinli

doi:10.1080/14767058.2017.1413548

Cited by 6 publications

(3 citation statements)

References 25 publications

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“…Oxygen glucose deprivation is widely used as a relatively convenient in vitro model for ischemia, stroke or HIE, showing similarities with the in vivo models of brain ischemia (Tasca et al, 2015). This primary neural cell or immortalized cell culture model has been used extensively to examine the cellular mechanisms mediating ischemia-reperfusion injury (Rousset et al, 2015;Gao et al, 2019). The OGD model is a simple process that firstly involves changes to the cell culture medium to exclude glucose.…”

Section: Oxygen Glucose Deprivationmentioning

confidence: 99%

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

Poupon-Bejuit

Rocha‐Ferreira

Thornton

et al. 2020

Front. Cell. Neurosci.

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Section: Oxygen Glucose Deprivationmentioning

confidence: 99%

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

Poupon-Bejuit

Rocha‐Ferreira

Thornton

et al. 2020

Front. Cell. Neurosci.

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“…We obtained primary microglial cells, according to a previously described technique [28,29]. Brie y, mixed glial cultures were prepared from newborn to 3-day-old Sprague-Dawley rat brains containing the cortex, hippocampus and striatum (CLEA Japan Inc., Tokyo, Japan) and cultured until con uent as described.…”

Section: Primary Microglial Cell Isolation From Newborn Rat Brainmentioning

confidence: 99%

LOX-1 Mediates Inflammatory Activation of Microglial Cells Through the p38-MAPK/NF-κB Pathways Under Hypoxic-Ischemic Conditions

Itoh¹,

Aoki²,

Akamatsu³

et al. 2020

Preprint

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Background: Microglial cells play an important role in the immune system in the brain. Activated microglial cells are not only injurious but also neuroprotective. We confirmed marked lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression in microglial cells in pathological lesions in the neonatal hypoxic-ischemic encephalopathy model brain. LOX-1 is known to be an activator of cytokines and chemokines through intracellular pathways. Here, we investigated a novel role of LOX-1 in microglial cells under hypoxic and ischemic conditions. Methods: We isolated primary rat microglial cells from 3-day-old Sprague-Dawley rat brains and confirmed that the isolated cells showed more than 98% Iba-1 positive with immunocytochemistry. We performed oxygen glucose deprivation (OGD) treatment of primary rat microglial cells as an in vitro model of nHIE. Then, we evaluated the expression levels of LOX-1, cytokines and chemokines with or without siRNA and inhibitors, compared with no OGD-treated cells. In addition, we analyzed reactive oxygen species and cell viability.Results: We found that defects in oxygen and nutrition induced LOX-1 expression and led to the production of inflammatory mediators, such as the cytokines IL-1β, IL-6 and TNF-α, the chemokines CCL2, CCL5 and CCL3 and reactive oxygen/nitrile species. Then, the LOX-1 signal transduction pathway was blocked by inhibitors, LOX-1 siRNA, the p38-MAPK inhibitor SB203580 and the NF-κB inhibitor BAY11-7082 suppressed the production of the inflammatory mediators. Moreover, we demonstrated that LOX-1 in microglial cells was autonomously overexpressed by positive feedback of the intracellular LOX-1 pathway. Conclusion: The hypoxic/ischemic conditions of microglial cells induced LOX-1 expression and activated immune system. We revealed one of the LOX-1 signaling pathways in microglia and provide a hint of a new treatment strategy for nHIE. It was speculated that Microglial cells are known to contribute to various neurological diseases. Hypoxic and ischemic brain injuries result in lifelong neurological and mental deficiency. LOX-1 and its related molecules or chemicals may be major therapeutic candidates.

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“…TH can prevent the development of brain edema, as well as reducing the damage produced by inflammation, oxidative stress and excitotoxicity [18]. Similarly, TH has also shown the ability to improve mitochondrial autophagy [106] and prevent apoptosis by preventing the translocation of the apoptosis-inducing factor (AIF) to the nucleus [165]. Some combined treatments approved for clinical trials involve EPO combined with hypothermia.…”

Section: Combined Therapies Using Thmentioning

confidence: 99%

Neuroprotective Role of Hypothermia in Hypoxic-ischemic Brain Injury: Combined Therapies using Estrogen

Toro-Urrego

Vesga-Jiménez

Herrera

et al. 2019

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Hypoxic-ischemic brain injury is a complex network of factors, which is mainly characterized by a decrease in levels of oxygen concentration and blood flow, which lead to an inefficient supply of nutrients to the brain. Hypoxic-ischemic brain injury can be found in perinatal asphyxia and ischemic-stroke, which represent one of the main causes of mortality and morbidity in children and adults worldwide. Therefore, knowledge of underlying mechanisms triggering these insults may help establish neuroprotective treatments. Selective Estrogen Receptor Modulators and Selective Tissue Estrogenic Activity Regulators exert several neuroprotective effects, including a decrease of reactive oxygen species, maintenance of cell viability, mitochondrial survival, among others. However, these strategies represent a traditional approach of targeting a single factor of pathology without satisfactory results. Hence, combined therapies, such as the administration of therapeutic hypothermia with a complementary neuroprotective agent, constitute a promising alternative. In this sense, the present review summarizes the underlying mechanisms of hypoxic-ischemic brain injury and compiles several neuroprotective strategies, including Selective Estrogen Receptor Modulators and Selective Tissue Estrogenic Activity Regulators, which represent putative agents for combined therapies with therapeutic hypothermia.

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Mild hypothermia protects neurons against oxygen glucose deprivation via poly (ADP-ribose) signaling

Abstract: These results showed that mild hypothermia partially protects immature hippocampal neurons against OGD injury in part by interfering with the PAR signaling pathway.

Cited by 6 publications

References 25 publications

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

Neuroprotective Effects of Diabetes Drugs for the Treatment of Neonatal Hypoxia-Ischemia Encephalopathy

LOX-1 Mediates Inflammatory Activation of Microglial Cells Through the p38-MAPK/NF-κB Pathways Under Hypoxic-Ischemic Conditions

Neuroprotective Role of Hypothermia in Hypoxic-ischemic Brain Injury: Combined Therapies using Estrogen

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