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 journalArticle

142 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)5026-5030
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number13
StatePublished - 1990

Fingerprint

Reperfusion Injury
Interleukin-1
Glutathione Disulfide
Glucosephosphate Dehydrogenase
Neutrophils
Vinblastine
Wounds and Injuries
Hydrogen Peroxide
Reperfusion
Oxidative Stress
Ischemia

Keywords

  • Antioxidants
  • Heart
  • Neutrophils
  • O radicals
  • Vascular injury

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Brown, J. M., White, C. W., Terada, L. S., Grosso, M. A., Shanley, P. F., Mulvin, D. W., ... Repine, J. E. (1990). Interleukin 1 pretreatment decreases ischemia/reperfusion injury. Proceedings of the National Academy of Sciences of the United States of America, 87(13), 5026-5030.

Interleukin 1 pretreatment decreases ischemia/reperfusion injury. / Brown, James M.; White, Carl W.; Terada, Lance S.; Grosso, Michael A.; Shanley, Paul F.; Mulvin, David W.; Banerjee, Anirban; Whitman, Glenn J R; Harken, Alden H.; Repine, John E.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 13, 1990, p. 5026-5030.

Research output: Contribution to journalArticle

Brown, JM, White, CW, Terada, LS, Grosso, MA, Shanley, PF, Mulvin, DW, Banerjee, A, Whitman, GJR, Harken, AH & Repine, JE 1990, 'Interleukin 1 pretreatment decreases ischemia/reperfusion injury', Proceedings of the National Academy of Sciences of the United States of America, vol. 87, no. 13, pp. 5026-5030.
Brown, James M. ; White, Carl W. ; Terada, Lance S. ; Grosso, Michael A. ; Shanley, Paul F. ; Mulvin, David W. ; Banerjee, Anirban ; Whitman, Glenn J R ; Harken, Alden H. ; Repine, John E. / Interleukin 1 pretreatment decreases ischemia/reperfusion injury. In: Proceedings of the National Academy of Sciences of the United States of America. 1990 ; Vol. 87, No. 13. pp. 5026-5030.
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AU - Mulvin, David W.

AU - Banerjee, Anirban

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AU - Harken, Alden H.

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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.

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