Indomethacin attenuates early increases in inducible heat shock protein 70 after cerebral ischemia/reperfusion in piglets

Tracy C. Beasley, F. Bari, Clara Thore, Nishadi Thrikawala, Thomas Louis, David Busija

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Indomethacin-sensitive mechanisms involved in inducible heat shock protein 70 (iHSP 70) synthesis were investigated at 6 h after global cerebral ischemia in parietal cortex and hippocampus. In anesthetized piglets, increased intracranial pressure was used to produce 5 or 10 min of cerebral ischemia. Brain regions were sampled for immunoblot analysis, immunohistochemistry and morphology. Immunoblots revealed differential expression of iHSP 70 in untreated brains. Cerebellum contained substantial amounts of iHSP 70 while lower levels were present in parietal cortex and hippocampus. Detectable increases in iHSP 70 were observed at 2 h after ischemia in parietal cortex and hippocampus. Using immunoblot data, calculation of percent change from control at 6 h after ischemia revealed significant (p <0.05) increases in iHSP 70 of 111 ± 39% (x̄ ± sem) (n = 6) in parietal cortex and 195 ± 69% (n = 8) in hippocampus. Increased iHSP 70 immunoreactivity occurred primarily in the granular/subgranular area of the dentate gyms 6 h after ischemia. Histological staining revealed little cellular injury at 6 h after ischemia in the granular/subgranular region injury whereas the CA3 region, which lacked iHSP 70 staining, displayed modest cellular injury. Cellular injury was also observed in cortical layers II/III and VI. At 6 h after ischemia, indomethacin pretreatment (5 mg/kg, i.v.) attenuated the iHSP 70 increases in parietal cortex and hippocampus (7 ± 30% and 89 ± 30%, respectively n = 5; p <0.05 compared to ischemia). Also, the increase in iHSP 70 immunoreactivity and appearance of cellular injury were not detected with indomethacin pretreatment. Thus, prior administration of indomethacin is associated with attenuation of ischemia- induced increases in iHSP 70 and cellular injury.

Original languageEnglish
Pages (from-to)125-135
Number of pages11
JournalDevelopmental Brain Research
Volume105
Issue number1
DOIs
Publication statusPublished - Jan 14 1998

Fingerprint

HSP70 Heat-Shock Proteins
Brain Ischemia
Indomethacin
Reperfusion
Parietal Lobe
Ischemia
Hippocampus
Wounds and Injuries
Staining and Labeling
Intracranial Pressure
Brain
Cerebellum
Immunohistochemistry

Keywords

  • Cyclooxygenase
  • Hippocampus
  • Morphology
  • Neonate
  • Parietal cortex
  • Stress protein

ASJC Scopus subject areas

  • Developmental Biology
  • Developmental Neuroscience

Cite this

Indomethacin attenuates early increases in inducible heat shock protein 70 after cerebral ischemia/reperfusion in piglets. / Beasley, Tracy C.; Bari, F.; Thore, Clara; Thrikawala, Nishadi; Louis, Thomas; Busija, David.

In: Developmental Brain Research, Vol. 105, No. 1, 14.01.1998, p. 125-135.

Research output: Contribution to journalArticle

Beasley, Tracy C. ; Bari, F. ; Thore, Clara ; Thrikawala, Nishadi ; Louis, Thomas ; Busija, David. / Indomethacin attenuates early increases in inducible heat shock protein 70 after cerebral ischemia/reperfusion in piglets. In: Developmental Brain Research. 1998 ; Vol. 105, No. 1. pp. 125-135.
@article{f849f7a0e68e4f3a9974b4dcecca32f3,
title = "Indomethacin attenuates early increases in inducible heat shock protein 70 after cerebral ischemia/reperfusion in piglets",
abstract = "Indomethacin-sensitive mechanisms involved in inducible heat shock protein 70 (iHSP 70) synthesis were investigated at 6 h after global cerebral ischemia in parietal cortex and hippocampus. In anesthetized piglets, increased intracranial pressure was used to produce 5 or 10 min of cerebral ischemia. Brain regions were sampled for immunoblot analysis, immunohistochemistry and morphology. Immunoblots revealed differential expression of iHSP 70 in untreated brains. Cerebellum contained substantial amounts of iHSP 70 while lower levels were present in parietal cortex and hippocampus. Detectable increases in iHSP 70 were observed at 2 h after ischemia in parietal cortex and hippocampus. Using immunoblot data, calculation of percent change from control at 6 h after ischemia revealed significant (p <0.05) increases in iHSP 70 of 111 ± 39{\%} (x̄ ± sem) (n = 6) in parietal cortex and 195 ± 69{\%} (n = 8) in hippocampus. Increased iHSP 70 immunoreactivity occurred primarily in the granular/subgranular area of the dentate gyms 6 h after ischemia. Histological staining revealed little cellular injury at 6 h after ischemia in the granular/subgranular region injury whereas the CA3 region, which lacked iHSP 70 staining, displayed modest cellular injury. Cellular injury was also observed in cortical layers II/III and VI. At 6 h after ischemia, indomethacin pretreatment (5 mg/kg, i.v.) attenuated the iHSP 70 increases in parietal cortex and hippocampus (7 ± 30{\%} and 89 ± 30{\%}, respectively n = 5; p <0.05 compared to ischemia). Also, the increase in iHSP 70 immunoreactivity and appearance of cellular injury were not detected with indomethacin pretreatment. Thus, prior administration of indomethacin is associated with attenuation of ischemia- induced increases in iHSP 70 and cellular injury.",
keywords = "Cyclooxygenase, Hippocampus, Morphology, Neonate, Parietal cortex, Stress protein",
author = "Beasley, {Tracy C.} and F. Bari and Clara Thore and Nishadi Thrikawala and Thomas Louis and David Busija",
year = "1998",
month = "1",
day = "14",
doi = "10.1016/S0165-3806(97)00179-X",
language = "English",
volume = "105",
pages = "125--135",
journal = "Developmental Brain Research",
issn = "0165-3806",
publisher = "Elsevier BV",
number = "1",

}

TY - JOUR

T1 - Indomethacin attenuates early increases in inducible heat shock protein 70 after cerebral ischemia/reperfusion in piglets

AU - Beasley, Tracy C.

AU - Bari, F.

AU - Thore, Clara

AU - Thrikawala, Nishadi

AU - Louis, Thomas

AU - Busija, David

PY - 1998/1/14

Y1 - 1998/1/14

N2 - Indomethacin-sensitive mechanisms involved in inducible heat shock protein 70 (iHSP 70) synthesis were investigated at 6 h after global cerebral ischemia in parietal cortex and hippocampus. In anesthetized piglets, increased intracranial pressure was used to produce 5 or 10 min of cerebral ischemia. Brain regions were sampled for immunoblot analysis, immunohistochemistry and morphology. Immunoblots revealed differential expression of iHSP 70 in untreated brains. Cerebellum contained substantial amounts of iHSP 70 while lower levels were present in parietal cortex and hippocampus. Detectable increases in iHSP 70 were observed at 2 h after ischemia in parietal cortex and hippocampus. Using immunoblot data, calculation of percent change from control at 6 h after ischemia revealed significant (p <0.05) increases in iHSP 70 of 111 ± 39% (x̄ ± sem) (n = 6) in parietal cortex and 195 ± 69% (n = 8) in hippocampus. Increased iHSP 70 immunoreactivity occurred primarily in the granular/subgranular area of the dentate gyms 6 h after ischemia. Histological staining revealed little cellular injury at 6 h after ischemia in the granular/subgranular region injury whereas the CA3 region, which lacked iHSP 70 staining, displayed modest cellular injury. Cellular injury was also observed in cortical layers II/III and VI. At 6 h after ischemia, indomethacin pretreatment (5 mg/kg, i.v.) attenuated the iHSP 70 increases in parietal cortex and hippocampus (7 ± 30% and 89 ± 30%, respectively n = 5; p <0.05 compared to ischemia). Also, the increase in iHSP 70 immunoreactivity and appearance of cellular injury were not detected with indomethacin pretreatment. Thus, prior administration of indomethacin is associated with attenuation of ischemia- induced increases in iHSP 70 and cellular injury.

AB - Indomethacin-sensitive mechanisms involved in inducible heat shock protein 70 (iHSP 70) synthesis were investigated at 6 h after global cerebral ischemia in parietal cortex and hippocampus. In anesthetized piglets, increased intracranial pressure was used to produce 5 or 10 min of cerebral ischemia. Brain regions were sampled for immunoblot analysis, immunohistochemistry and morphology. Immunoblots revealed differential expression of iHSP 70 in untreated brains. Cerebellum contained substantial amounts of iHSP 70 while lower levels were present in parietal cortex and hippocampus. Detectable increases in iHSP 70 were observed at 2 h after ischemia in parietal cortex and hippocampus. Using immunoblot data, calculation of percent change from control at 6 h after ischemia revealed significant (p <0.05) increases in iHSP 70 of 111 ± 39% (x̄ ± sem) (n = 6) in parietal cortex and 195 ± 69% (n = 8) in hippocampus. Increased iHSP 70 immunoreactivity occurred primarily in the granular/subgranular area of the dentate gyms 6 h after ischemia. Histological staining revealed little cellular injury at 6 h after ischemia in the granular/subgranular region injury whereas the CA3 region, which lacked iHSP 70 staining, displayed modest cellular injury. Cellular injury was also observed in cortical layers II/III and VI. At 6 h after ischemia, indomethacin pretreatment (5 mg/kg, i.v.) attenuated the iHSP 70 increases in parietal cortex and hippocampus (7 ± 30% and 89 ± 30%, respectively n = 5; p <0.05 compared to ischemia). Also, the increase in iHSP 70 immunoreactivity and appearance of cellular injury were not detected with indomethacin pretreatment. Thus, prior administration of indomethacin is associated with attenuation of ischemia- induced increases in iHSP 70 and cellular injury.

KW - Cyclooxygenase

KW - Hippocampus

KW - Morphology

KW - Neonate

KW - Parietal cortex

KW - Stress protein

UR - http://www.scopus.com/inward/record.url?scp=0032515387&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032515387&partnerID=8YFLogxK

U2 - 10.1016/S0165-3806(97)00179-X

DO - 10.1016/S0165-3806(97)00179-X

M3 - Article

C2 - 9497086

AN - SCOPUS:0032515387

VL - 105

SP - 125

EP - 135

JO - Developmental Brain Research

JF - Developmental Brain Research

SN - 0165-3806

IS - 1

ER -