Interleukin 1 pretreatment decreases ischemia/reperfusion injury

James M. Brown; Carl W. White; Lance S. Terada; Michael A. Grosso; Paul F. Shanley; David W. Mulvin; Anirban Banerjee; Glenn J.R. Whitman; Alden H. Harken; John E. Repine

Interleukin 1 pretreatment decreases ischemia/reperfusion injury

James M. Brown, Carl W. White, Lance S. Terada, Michael A. Grosso, Paul F. Shanley, David W. Mulvin, Anirban Banerjee, Glenn J.R. Whitman, Alden H. Harken, John E. Repine

Research output: Contribution to journal › Article › peer-review

143 Scopus citations

Abstract

Hearts isolated from rats treated 36 hr before with interleukin 1 (IL-1) had increased glucose-6-phosphate dehydrogenase (G6PD) activity and decreased hydrogen peroxide levels and injury after global ischemia (I, 20 min)/reperfusion (R, 40 min) compared with hearts from untreated rats. Hearts isolated from rats treated 6 hr earlier with IL-1 also had increased polymorphonuclear leukocytes (PMN), H₂O₂ levels, and oxidized glutathione (GSSG) contents compared with hearts from untreated rats. Depletion of circulating blood PMN by prior treatment with vinblastine prevented both early (from treatment 6 hr before study) IL-1-induced increases in myocardial PMN accumulation, H₂O₂ levels, and GSSG contents and late (from treatment 36 hr before study) increases in myocardial G6PD activity and protection against I/R. Our results indicate that IL-1 pretreatment causes an early (6 hr after IL-1 treatment) myocardial PMN accumulation and most likely an H₂O₂-dependent oxidative stress, which contributes to late (36 hr after IL-1 treatment) increases in myocardial G6PD activity and decreases in I/R injury.

Original language	English (US)
Pages (from-to)	5026-5030
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	87
Issue number	13
State	Published - 1990
Externally published	Yes

Keywords

Antioxidants
Heart
Neutrophils
O radicals
Vascular injury

ASJC Scopus subject areas

General

Cite this

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title = "Interleukin 1 pretreatment decreases ischemia/reperfusion injury",

abstract = "Hearts isolated from rats treated 36 hr before with interleukin 1 (IL-1) had increased glucose-6-phosphate dehydrogenase (G6PD) activity and decreased hydrogen peroxide levels and injury after global ischemia (I, 20 min)/reperfusion (R, 40 min) compared with hearts from untreated rats. Hearts isolated from rats treated 6 hr earlier with IL-1 also had increased polymorphonuclear leukocytes (PMN), H2O2 levels, and oxidized glutathione (GSSG) contents compared with hearts from untreated rats. Depletion of circulating blood PMN by prior treatment with vinblastine prevented both early (from treatment 6 hr before study) IL-1-induced increases in myocardial PMN accumulation, H2O2 levels, and GSSG contents and late (from treatment 36 hr before study) increases in myocardial G6PD activity and protection against I/R. Our results indicate that IL-1 pretreatment causes an early (6 hr after IL-1 treatment) myocardial PMN accumulation and most likely an H2O2-dependent oxidative stress, which contributes to late (36 hr after IL-1 treatment) increases in myocardial G6PD activity and decreases in I/R injury.",

keywords = "Antioxidants, Heart, Neutrophils, O radicals, Vascular injury",

author = "Brown, {James M.} and White, {Carl W.} and Terada, {Lance S.} and Grosso, {Michael A.} and Shanley, {Paul F.} and Mulvin, {David W.} and Anirban Banerjee and Whitman, {Glenn J.R.} and Harken, {Alden H.} and Repine, {John E.}",

year = "1990",

language = "English (US)",

volume = "87",

pages = "5026--5030",

journal = "Proceedings of the National Academy of Sciences of the United States of America",

issn = "0027-8424",

publisher = "National Academy of Sciences",

number = "13",

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TY - JOUR

T1 - Interleukin 1 pretreatment decreases ischemia/reperfusion injury

AU - Brown, James M.

AU - White, Carl W.

AU - Terada, Lance S.

AU - Grosso, Michael A.

AU - Shanley, Paul F.

AU - Mulvin, David W.

AU - Banerjee, Anirban

AU - Whitman, Glenn J.R.

AU - Harken, Alden H.

AU - Repine, John E.

PY - 1990

Y1 - 1990

N2 - Hearts isolated from rats treated 36 hr before with interleukin 1 (IL-1) had increased glucose-6-phosphate dehydrogenase (G6PD) activity and decreased hydrogen peroxide levels and injury after global ischemia (I, 20 min)/reperfusion (R, 40 min) compared with hearts from untreated rats. Hearts isolated from rats treated 6 hr earlier with IL-1 also had increased polymorphonuclear leukocytes (PMN), H2O2 levels, and oxidized glutathione (GSSG) contents compared with hearts from untreated rats. Depletion of circulating blood PMN by prior treatment with vinblastine prevented both early (from treatment 6 hr before study) IL-1-induced increases in myocardial PMN accumulation, H2O2 levels, and GSSG contents and late (from treatment 36 hr before study) increases in myocardial G6PD activity and protection against I/R. Our results indicate that IL-1 pretreatment causes an early (6 hr after IL-1 treatment) myocardial PMN accumulation and most likely an H2O2-dependent oxidative stress, which contributes to late (36 hr after IL-1 treatment) increases in myocardial G6PD activity and decreases in I/R injury.

AB - Hearts isolated from rats treated 36 hr before with interleukin 1 (IL-1) had increased glucose-6-phosphate dehydrogenase (G6PD) activity and decreased hydrogen peroxide levels and injury after global ischemia (I, 20 min)/reperfusion (R, 40 min) compared with hearts from untreated rats. Hearts isolated from rats treated 6 hr earlier with IL-1 also had increased polymorphonuclear leukocytes (PMN), H2O2 levels, and oxidized glutathione (GSSG) contents compared with hearts from untreated rats. Depletion of circulating blood PMN by prior treatment with vinblastine prevented both early (from treatment 6 hr before study) IL-1-induced increases in myocardial PMN accumulation, H2O2 levels, and GSSG contents and late (from treatment 36 hr before study) increases in myocardial G6PD activity and protection against I/R. Our results indicate that IL-1 pretreatment causes an early (6 hr after IL-1 treatment) myocardial PMN accumulation and most likely an H2O2-dependent oxidative stress, which contributes to late (36 hr after IL-1 treatment) increases in myocardial G6PD activity and decreases in I/R injury.

KW - Antioxidants

KW - Heart

KW - Neutrophils

KW - O radicals

KW - Vascular injury

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Interleukin 1 pretreatment decreases ischemia/reperfusion injury

Abstract

Keywords

ASJC Scopus subject areas

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