Effects of anoxic stress on prostaglandin H synthase isoforms in piglet brain

被引:27
作者
Dégì, R
Bari, F
Thrikawala, N
Beasley, TC
Thore, C
Louis, TM
Busija, DW
机构
[1] Wake Forest Univ, Bowman Gray Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27157 USA
[2] Albert Szent Gyorgyi Med Univ, Dept Ophthalmol, H-6701 Szeged, Hungary
[3] Albert Szent Gyorgyi Med Univ, Dept Physiol, H-6701 Szeged, Hungary
[4] E Carolina Univ, Sch Med, Dept Anat & Cell Biol, Greenville, NC 27858 USA
来源
DEVELOPMENTAL BRAIN RESEARCH | 1998年 / 107卷 / 02期
关键词
cyclooxygenase; cerebral cortex; hippocampus; cerebellum; ischemia; asphyxia; prostaglandin H synthase-1; prostaglandin H synthase-2; indomethacin; nitric oxide synthase;
D O I
10.1016/S0165-3806(98)00022-4
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
We examined effects of ischemia and asphyxia on levels of prostaglandin H synthase-l (PGHS-1) and prostaglandin H synthase-2 (PGHS-2) in piglet brain. Ischemia was induced by increasing intracranial pressure and asphyxia was induced by turning off the respirator. Duration of anoxic stress was 10 min. In some animals, indomethacin (5 mg/kg, i.v.) or 7-nitroindazole (7-NI) was administered prior to ischemia to block PGHS or brain nitric oxide synthase (bNOS), respectively. Tissues from cerebral cortex and hippocampus were removed and fixed and/or frozen after 1, 2, 4 and 8 h of recovery from anoxic stress. In addition, tissues were obtained from untreated animals or from time control animals. Levels of mRNA and proteins were determined using RNase protection assay and immunohistochemical approaches, respectively. In the tissues studied, only a few neurons were immunopositive for PGHS-1, and neither ischemia or asphyxia affected PGHS-1 immunostaining at 8 h after recovery. Likewise, PGHS-1 mRNA did not increase following anoxic stress. In contrast, substantial PGHS-2 immunoreactivity was present in neurons and glial cells in the cerebral cortex and hippocampus and there was no difference between time control and non treated animals. PGHS-2 mRNA increased by 2-4 h after ischemia, and heightened immunoreactivity for PGHS-2 was present at 8 h after ischemia in cerebral cortex and hippocampus. However, asphyxia did not increase PGHS-2 mRNA or immunostaining. Indomethacin pretreatment inhibited increases in mRNA and protein for PGHS-2 after ischemia, while 7-NI had little effect on increases in PGHS-2 immunoreactivity. We conclude that: (1) PGHS-2 is the predominant isoform present in piglet cerebral cortex and hippocampus; (2) Ischemia but not asphyxia increases levels of PGHS-2; (3) Ischemia does-not increase levels of PGHS-1; and (4) Indomethacin but not 7-NI attenuates ischemia-induced increases in PGHS-2. (C) 1998 Elsevier Science B.V.
引用
收藏
页码:265 / 276
页数:12
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