Microglia activation after neonatal hypoxic-ischemia

McRae, Amanda; Gilland, Eric; Bona, Elsa; Hagberg, Henrik

doi:10.1016/0165-3806(94)00177-2

Cited by 191 publications

(119 citation statements)

References 32 publications

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“…On the contrary, under the condition of hypoglycemia and hypoxemia by HI insult, IL-1␤ directly or indirectly attacks neurons and leads to neuronal cell death (34). Moreover, IL-1␤ induces microglial activation in cortex 3-4 d after HI in the neonatal rat (35,36). This cycle causes many neuronal cell deaths and expansion of lesions.…”

Section: Discussionmentioning

confidence: 99%

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

et al. 2009

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Neonatal hypoxic-ischemic encephalopathy (HIE) is the most frequent neurologic disease in the perinatal period. Its major cause is oxidative stress, which induces DNA peroxidation and apoptotic neuronal death. We examined 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) expression to evaluate brain damage in neonatal HIE and the therapeutic effect of edaravone, a free radical scavenger. Using HPLC and immunohistochemistry, the 8-OHdG levels of neonatal HIE model Sprague-Dawley rats that were subjected to left common carotid artery ligation and 2-h hypoxia significantly increased after 24 -48 h of hypoxic-ischemic (HI) insult, but decreased after 72 h. Moreover, the number of apoptotic cells with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and karyorrhexis significantly increased after 24 -72 h of HI insult. In a therapeutic experiment, edaravone was administered i.p.

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Section: Discussionmentioning

confidence: 99%

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

et al. 2009

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“…In our model, a significant increase of ameboid microglia occurred between 24 and 72 hours postischemia, during the window of vulnerability to selective HI white matter injury, as compared to controls. In the P7 rat, microglia have been implicated in the pathophysiology of neonatal injuries with a transient increase in microglial antigens between 24 hours and 3-4 days post HI in P7 rats (McRae et al, 1995), and after excitotoxic lesions of the developing murine periventricular white matter (Tahraoui et al, 2001). Here, we demonstrated that i) early NG2-positive OLs matured into O4-positive OLs in the cingulum and were also present at the vicinity of the cyst, and ii) increased macrophage/microglia phagocytosed O4-positive OLs, suggesting that the presence of activated microglia interferes with the maturation of immature OLs leading to impaired remyelination.…”

Section: Discussionmentioning

confidence: 99%

Glial activation in white matter following ischemia in the neonatal P7 rat brain

Biran

Joly

Héron

et al. 2006

Experimental Neurology

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This study examines cell death and proliferation in the white matter after neonatal stroke. In post-natal day 7 injured rat, there was a marked reduction in myelin basic protein (MBP) immunostaining mainly corresponding to numerous pyknotic immature oligodendrocytes and TUNEL-positive astrocytes in the ipsilateral external capsule. In contrast, a substantial restoration of MBP, as indicated by the MBP ratio of left-toright, occurred in the cingulum at 48 (1.27 ± 0.12) and 72 (1.30 ± 0.18, p<0.05) hours of recovery as compared to age-matched controls (1.03 ± 0.14). Ki-67 immunostaining revealed a first peak of newly-generated cells in the dorsolateral hippocampal subventricular zone and cingulum at 72 hours after reperfusion. Double immunofluorescence revealed that most of the Ki-67-positive cells were astrocytes at 48 hours and NG2 pre-oligodendrocytes at 72 hours of recovery. Microglia infiltration occurs over several days in the cingulum and a huge quantity of macrophages reached the subcortical white matter where they engulfed immature oligodendrocytes. The overall results suggest that the persistent activation of microglia involves a chronic component of immunoinflammation, which overwhelms repair processes and contributes to cystic growth in the developing brain.

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“…Newborn animal studies have shown that the inflammatory response following hypoxia occurs relatively early, with increased cerebral expression of inflammatory genes and microglial activation already 2-3 hours after the insult [97][98][99] . In clinical studies, increased cytokine levels were detected during the first 1-4 days after asphyxia in the cerebrospinal fluid (CSF) 100,101 , in umbilical cord blood 102 and in serum 103 .…”

Section: Inflammationmentioning

confidence: 99%

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

et al. 2009

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Microglia activation after neonatal hypoxic-ischemia

Cited by 191 publications

References 32 publications

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

Edaravone Inhibits DNA Peroxidation and Neuronal Cell Death in Neonatal Hypoxic-Ischemic Encephalopathy Model Rat

Glial activation in white matter following ischemia in the neonatal P7 rat brain

Post-hypoxic hypothermia is protective in human NT2-N neurons regardless of oxygen concentration during reoxygenation

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