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Published online before print December 5, 2005

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(Journal of Leukocyte Biology. 2006;79:277-284.)
© 2006 by Society for Leukocyte Biology

Mechanism of the salutary effects of flutamide on intestinal myeloperoxidase activity following trauma-hemorrhage: up-regulation of estrogen receptor-ß-dependent HO-1

Huang-Ping Yu^*,, Mashkoor A. Choudhry^*, Tomoharu Shimizu^*, Ya-Ching Hsieh^*, Martin G. Schwacha^*, Shaolong Yang^* and Irshad H. Chaudry^*,1

^* Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham; and
Graduate Institute of Clinical Medical Sciences, Chang Gung University, Taoyuan, Taiwan

¹ Correspondence: Center for Surgical Research, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall, Room G094, Birmingham, AL 35294-0019. E-mail: Irshad.Chaudry{at}ccc.uab.edu

Hemeoxygenase (HO)-1 induction following adverse circulatory conditions is known to be protective, and precastrated males have less intestinal damage than sham-operated males following trauma-hemorrhage (T-H). Previous studies have also shown that administration of flutamide up-regulated estrogen receptor (ER) expression in males following T-H. We hypothesized that flutamide administration in males following T-H up-regulates HO-1 via an ER-dependent pathway and protects against intestinal injury. Male Sprague-Dawley rats underwent T-H [mean blood pressure (MBP) 40 mmHg for 90 min and then resuscitation]. A single dose of flutamide (25 mg/kg body weight), with or without an ER antagonist (ICI 182,780), a HO enzyme inhibitor [chromium-mesoporphyrin (CrMP)], or vehicle, was administered subcutaneously during resuscitation. At 2 h after T-H or sham operation, intestinal myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM)-1, cytokine-induced neutrophil chemoattractant (CINC)-1, and CINC-3 levels were measured. Intestinal ER-, ER-ß, androgen receptor, and HO-1 mRNA/protein levels were also determined. Results showed that T-H increased intestinal MPO activity, ICAM-1, CINC-1, and CINC-3 levels. These parameters were improved significantly in the flutamide-treated rats subjected to T-H. Flutamide treatment increased intestinal HO-1 and ER-ß mRNA/protein levels as compared with vehicle-treated T-H rats. Administration of the ER antagonist ICI 182,780 or the HO inhibitor CrMP prevented the flutamide-induced attenuation of shock-induced intestinal damage. Thus, the salutary effects of flutamide administration on attenuation of intestinal injury following T-H are mediated via up-regulation of ER-ß-dependent HO-1 expression.

Key Words: chromium-mesoporphyrin • hemorrhagic shock • ICAM-1 • CINC-1 • CINC-3

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