Postischemic Hyperthermia Induced Caspase-3 Activation in the Newborn Rat Brain after Hypoxia-Ischemia and Exacerbated the Brain Damage

Neonatology ◽  
2003 ◽  
Vol 84 (2) ◽  
pp. 164-171 ◽  
Author(s):  
Hirotsugu Fukuda ◽  
Takuji Tomimatsu ◽  
Takeshi Kanagawa ◽  
Junwu Mu ◽  
Masatomo Kohzuki ◽  
...  
Keyword(s):  
Rat Brain ◽  
Brain Damage ◽  
Caspase 3 ◽  
Newborn Rat ◽  
Hypoxia Ischemia ◽  
The Brain

Hypoxia-Ischemia, but Not Hypoxia Alone, Induces the Expression of Heme Oxygenase-1 (HSP32) in Newborn Rat Brain

1997 ◽  
Vol 17 (6) ◽  
pp. 647-658 ◽  
Author(s):  
Marcelle Bergeron ◽  
Donna M. Ferriero ◽  
Hendrik J. Vreman ◽  
David K. Stevenson ◽  
Frank R. Sharp
Keyword(s):  
Rat Brain ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1 ◽  
Bile Pigments ◽  
Newborn Rat ◽  
Brain Macrophages ◽  
Rat Pups ◽  
Hypoxia Ischemia ◽  
Wistar Kyoto ◽  
The Brain

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme to produce bile pigments and carbon monoxide. The HO-1 isozyme is induced by a variety of agents such as heat, heme, and hydrogen peroxide. Evidence suggests that the bile pigments serve as antioxidants in cells with compromised defense mechanisms. Because hypoxia-ischemia (HI) increases the level of oxygen free radicals, the induction of HO-1 expression in the brain during ischemia could modulate the response to oxidative stress. To study the possible involvement of HO-1 in neonatal hypoxia-induced ischemic tolerance, we examined the brains of newborn rat pups exposed to 8% O2 (for 2.5 to 3 hours), and the brain of chronically hypoxic rat pups with congenital cardiac defects (Wistar Kyoto; WKY/ NCr). Heme oxygenase-1 immunostaining did not change after either acute or chronic hypoxia, suggesting that HO-1 is not a good candidate for explaining hypoxia preconditioning in newborn rat brain. To study the role of HO-1 in neonatal HI, 1-week-old rats were subjected to right carotid coagulation and exposure to 8% O2/92% N2 for 2.5 hours. Whereas HO enzymatic activity was unchanged in ipsilateral cortex and subcortical regions compared with the contralateral hemisphere or control brains, immunocytochemistry and Western blot analysis showed increased HO-1 staining in ipsilateral cortex, hippocampus, and striatum at 12 to 24 hours up to 7 days after HI. Double fluorescence immunostaining showed that HO-1 was expressed mostly in ED-1 positive macrophages. Because activated brain macrophages have been associated with the release of several cytotoxic molecules, the presence of HO-1 positive brain macrophages may determine the tissue vulnerability after HI injury.

Post-ischemic hypothermia blocks caspase-3 activation in the newborn rat brain after hypoxia–ischemia

2001 ◽  
Vol 910 (1-2) ◽  
pp. 187-191 ◽  
Author(s):  
Hirotsugu Fukuda ◽  
Takuji Tomimatsu ◽  
Noriyoshi Watanabe ◽  
Jun Wu Mu ◽  
Masatomo Kohzuki ◽  
...  
Keyword(s):  
Rat Brain ◽  
Caspase 3 ◽  
Newborn Rat ◽  
Hypoxia Ischemia

Subcellular Distribution of DNA Polymerase Activity in Newborn Rat Brain and Liver

1971 ◽  
Vol 49 (12) ◽  
pp. 1285-1291 ◽  
Author(s):  
M. R. V. Murthy ◽  
A. D. Bharucha
Keyword(s):  
Enzyme Activity ◽  
Rat Brain ◽  
Dna Polymerase ◽  
Subcellular Fraction ◽  
Polymerase Activity ◽  
Particulate Material ◽  
Newborn Rat ◽  
Newborn Brain ◽  
Rat Brain And Liver ◽  
The Brain

DNA polymerase activities were determined in the cytoplasmic soluble, the nuclear soluble, and the nuclear particulate fractions of newborn rat brain and liver. The results indicate that a majority of the brain nuclear enzyme may be bound to particulate material while a majority of the liver nuclear enzyme may be free or only loosely bound. Although the subcellular distributions of DNA polymerase activity are widely different in newborn brain and liver, the enzyme activity in any given subcellular fraction is higher in liver than in brain.

scholarly journals Serum 24S-hydroxycholesterol predicts long-term brain structural and functional outcomes after hypoxia-ischemia in neonatal mice

2020 ◽  
pp. 0271678X2091191 ◽  
Author(s):  
Fuxin Lu ◽  
Shujuan Fan ◽  
Andrea R Romo ◽  
Duan Xu ◽  
Donna M Ferriero ◽  
...  
Keyword(s):  
Brain Damage ◽  
Functional Outcomes ◽  
Cholesterol Metabolism ◽  
Blue Staining ◽  
Functional Impairments ◽  
Major Pathway ◽  
Hypoxia Ischemia ◽  
Severe Motor ◽  
The Brain

The major pathway of brain cholesterol turnover relies on its hydroxylation into 24S-hydroxycholesterol (24S-HC) using brain-specific cytochrome P450 46A1 (CYP46A1). 24S-HC produced exclusively in the brain normally traverses the blood-brain barrier to enter the circulation to the liver for excretion; therefore, the serum 24S-HC level is an indication of cholesterol metabolism in the brain. We recently reported an upregulation of CYP46A1 following hypoxia-ischemia (HI) in the neonatal mouse brain and a correlation between serum 24S-HC levels and acute brain damage. Here, we performed a longitudinal study to investigate whether the serum 24S-HC concentrations predict long-term brain structural and functional outcomes. In postnatal day 9 mice subjected to HI, the serum 24S-HC levels increased at 6 h and 24 h after HI and correlated with the infarct volumes measured histologically or by T2-weighted MRI. The 24 h levels were associated with white matter volume loss quantified by MBP immunostaining and luxol fast blue staining. The animals with higher serum 24S-HC at 6 h and 24 h corresponded to those with more severe motor and cognitive deficits at 35-40 days after HI. These data suggest that 24S-HC could be a novel and early blood biomarker for severity of neonatal HI brain damage and associated functional impairments.

Measuring the Accentuation of the Brain Damage That Arises from Perinatal Cerebral Hypoxia-Ischemia

Neonatology ◽  
1997 ◽  
Vol 72 (3) ◽  
pp. 187-191 ◽  
Author(s):  
Robert C. Vannucci ◽  
Anthony Rossini ◽  
Javad Towfighi ◽  
Susan J. Vannucci
Keyword(s):  
Brain Damage ◽  
Cerebral Hypoxia ◽  
Hypoxia Ischemia ◽  
The Brain

Amelioration by glycine of brain damage in neonatal rat brain following hypoxia-ischemia

2017 ◽  
Vol 59 (3) ◽  
pp. 321-327 ◽  
Author(s):  
Hiroko Mori ◽  
Ken Momosaki ◽  
Jun Kido ◽  
Tetsuo Naramura ◽  
Kenichi Tanaka ◽  
...  
Keyword(s):  
Rat Brain ◽  
Brain Damage ◽  
Neonatal Rat ◽  
Hypoxia Ischemia ◽  
Neonatal Rat Brain
Sign in / Sign up

Export Citation Format

Share Document