Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock

  • Authors:
    • Yutaka Arimori
    • Toru Takahashi
    • Hiroyuki Nishie
    • Kazuyoshi Inoue
    • Hiroko Shimizu
    • Emiko Omori
    • Susumu Kawanishi
    • Yuichiro Toda
    • Hiroshi Morimatsu
    • Kiyoshi Morita
  • View Affiliations

  • Published online on: July 1, 2010     https://doi.org/10.3892/ijmm_00000430
  • Pages: 27-32
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Abstract

Hemorrhagic shock followed by resuscitation (HSR) causes oxidative stress, which results in multiple organ damage. The kidney is one of the target organs of HSR-mediated oxidative tissue injury. Heme oxygenase (HO)-1, the rate-limiting enzyme in heme catabolism, is induced by oxidative stress; it protects against oxidative tissue injuries. The aim of the present study was to examine the role of renal HO-1 induction after HSR. Rats were subjected to hemorrhagic shock to achieve a mean arterial pressure of 30 mmHg for 60 min, followed by resuscitation with the shed blood. HSR resulted in a significant increase in functional HO-1 protein in the tubular epithelial cells of the kidney, whereas HSR resulted in only a slight increase in gene expression of tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS), and in protein expression of activated caspase-3 solely in renal cells where HO-1 expression was absent. HSR also resulted in a significant increase in Bcl-2 gene expression. Pretreatment of HSR animals with tin-mesoporphyrin (0.5 µmol/kg), a specific competitive inhibitor of HO activity, resulted in a significant decrease in HO activity and exacerbated tissue inflammation and apoptotic cell death as judged by the marked increase in expression of TNF-α and iNOS, and in activated caspase-3-positive cells, and the significant reduction in Bcl-2 expression, respectively. These findings indicate that HO-1 induction is an adaptive response to HSR-induced oxidative stress and is essential for protecting tubular epithelial cells from oxidative damage through its anti-inflammatory and anti-apoptotic properties.

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July 2010
Volume 26 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Arimori Y, Takahashi T, Nishie H, Inoue K, Shimizu H, Omori E, Kawanishi S, Toda Y, Morimatsu H, Morita K, Morita K, et al: Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock. Int J Mol Med 26: 27-32, 2010
APA
Arimori, Y., Takahashi, T., Nishie, H., Inoue, K., Shimizu, H., Omori, E. ... Morita, K. (2010). Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock. International Journal of Molecular Medicine, 26, 27-32. https://doi.org/10.3892/ijmm_00000430
MLA
Arimori, Y., Takahashi, T., Nishie, H., Inoue, K., Shimizu, H., Omori, E., Kawanishi, S., Toda, Y., Morimatsu, H., Morita, K."Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock". International Journal of Molecular Medicine 26.1 (2010): 27-32.
Chicago
Arimori, Y., Takahashi, T., Nishie, H., Inoue, K., Shimizu, H., Omori, E., Kawanishi, S., Toda, Y., Morimatsu, H., Morita, K."Role of heme oxygenase-1 in protection of the kidney after hemorrhagic shock". International Journal of Molecular Medicine 26, no. 1 (2010): 27-32. https://doi.org/10.3892/ijmm_00000430