Postischemic treatment with aminoguanidine inhibits peroxynitrite production in the rat hippocampus following transient forebrain ischemia

Yun Sik Choi, Yeo Hong Yoon, Ju Eun Lee, Kyung Ok Cho, Seong Yun Kim, Sang Bok Lee

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippocampus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or saline (0.4 ml/100 g, i.p.) was started 30 min following ischemia-reperfusion and the animals were then injected twice daily until 12 h before sacrifice. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. Posttreatment of aminoguanidine (200 mg/kg) significantly attenuated the neuronal death in the hippocampal CA1 area 3 days, but not 7 days, after ischemia-reperfusion. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion, which was prevented by the treatment of aminoguanidine (100 mg/kg and 200 mg/kg). Our findings showed that (1) the generation of peroxynitrite in the hippocampal CA1 area 3 days after ischemia-reperfusion was dependent on the iNOS activity; (2) the postischemic delayed neuronal death was attenuated in the early phase through the prevention of peroxynitrite generation by an iNOS inhibitor.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalKorean Journal of Physiology and Pharmacology
Volume8
Issue number1
StatePublished - Feb 2004

Fingerprint

Peroxynitrous Acid
Prosencephalon
Hippocampus
Ischemia
Reperfusion
pimagedine

Keywords

  • Aminoguanidine
  • Hippocampus
  • iNOS
  • Peroxynitrite
  • Rats
  • Transient forebrain ischemia

ASJC Scopus subject areas

  • Pharmacology
  • Physiology

Cite this

Postischemic treatment with aminoguanidine inhibits peroxynitrite production in the rat hippocampus following transient forebrain ischemia. / Choi, Yun Sik; Yoon, Yeo Hong; Lee, Ju Eun; Cho, Kyung Ok; Kim, Seong Yun; Lee, Sang Bok.

In: Korean Journal of Physiology and Pharmacology, Vol. 8, No. 1, 02.2004, p. 1-5.

Research output: Contribution to journalArticle

Choi, Yun Sik ; Yoon, Yeo Hong ; Lee, Ju Eun ; Cho, Kyung Ok ; Kim, Seong Yun ; Lee, Sang Bok. / Postischemic treatment with aminoguanidine inhibits peroxynitrite production in the rat hippocampus following transient forebrain ischemia. In: Korean Journal of Physiology and Pharmacology. 2004 ; Vol. 8, No. 1. pp. 1-5.
@article{7bba686de1df450382c6d376f160cb10,
title = "Postischemic treatment with aminoguanidine inhibits peroxynitrite production in the rat hippocampus following transient forebrain ischemia",
abstract = "Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippocampus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or saline (0.4 ml/100 g, i.p.) was started 30 min following ischemia-reperfusion and the animals were then injected twice daily until 12 h before sacrifice. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. Posttreatment of aminoguanidine (200 mg/kg) significantly attenuated the neuronal death in the hippocampal CA1 area 3 days, but not 7 days, after ischemia-reperfusion. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion, which was prevented by the treatment of aminoguanidine (100 mg/kg and 200 mg/kg). Our findings showed that (1) the generation of peroxynitrite in the hippocampal CA1 area 3 days after ischemia-reperfusion was dependent on the iNOS activity; (2) the postischemic delayed neuronal death was attenuated in the early phase through the prevention of peroxynitrite generation by an iNOS inhibitor.",
keywords = "Aminoguanidine, Hippocampus, iNOS, Peroxynitrite, Rats, Transient forebrain ischemia",
author = "Choi, {Yun Sik} and Yoon, {Yeo Hong} and Lee, {Ju Eun} and Cho, {Kyung Ok} and Kim, {Seong Yun} and Lee, {Sang Bok}",
year = "2004",
month = "2",
language = "English (US)",
volume = "8",
pages = "1--5",
journal = "Korean Journal of Physiology and Pharmacology",
issn = "1226-4512",
publisher = "Korean Physiological Soc. and Korean Soc. of Pharmacology",
number = "1",

}

TY - JOUR

T1 - Postischemic treatment with aminoguanidine inhibits peroxynitrite production in the rat hippocampus following transient forebrain ischemia

AU - Choi, Yun Sik

AU - Yoon, Yeo Hong

AU - Lee, Ju Eun

AU - Cho, Kyung Ok

AU - Kim, Seong Yun

AU - Lee, Sang Bok

PY - 2004/2

Y1 - 2004/2

N2 - Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippocampus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or saline (0.4 ml/100 g, i.p.) was started 30 min following ischemia-reperfusion and the animals were then injected twice daily until 12 h before sacrifice. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. Posttreatment of aminoguanidine (200 mg/kg) significantly attenuated the neuronal death in the hippocampal CA1 area 3 days, but not 7 days, after ischemia-reperfusion. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion, which was prevented by the treatment of aminoguanidine (100 mg/kg and 200 mg/kg). Our findings showed that (1) the generation of peroxynitrite in the hippocampal CA1 area 3 days after ischemia-reperfusion was dependent on the iNOS activity; (2) the postischemic delayed neuronal death was attenuated in the early phase through the prevention of peroxynitrite generation by an iNOS inhibitor.

AB - Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippocampus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or saline (0.4 ml/100 g, i.p.) was started 30 min following ischemia-reperfusion and the animals were then injected twice daily until 12 h before sacrifice. Immunohistochemical method was used to detect 3-nitrotyrosine, a marker of peroxynitrite production. Posttreatment of aminoguanidine (200 mg/kg) significantly attenuated the neuronal death in the hippocampal CA1 area 3 days, but not 7 days, after ischemia-reperfusion. 3-Nitrotyrosine immunoreactivity was enhanced in the hippocampal CA1 area 3 days after reperfusion, which was prevented by the treatment of aminoguanidine (100 mg/kg and 200 mg/kg). Our findings showed that (1) the generation of peroxynitrite in the hippocampal CA1 area 3 days after ischemia-reperfusion was dependent on the iNOS activity; (2) the postischemic delayed neuronal death was attenuated in the early phase through the prevention of peroxynitrite generation by an iNOS inhibitor.

KW - Aminoguanidine

KW - Hippocampus

KW - iNOS

KW - Peroxynitrite

KW - Rats

KW - Transient forebrain ischemia

UR - http://www.scopus.com/inward/record.url?scp=1542286036&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1542286036&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:1542286036

VL - 8

SP - 1

EP - 5

JO - Korean Journal of Physiology and Pharmacology

JF - Korean Journal of Physiology and Pharmacology

SN - 1226-4512

IS - 1

ER -