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This Article Full Text Full Text (PDF) All Versions of this Article: 290/5/L1004    most recent 00504.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Yu, H.-P. Articles by Chaudry, I. H. Search for Related Content PubMed PubMed Citation Articles by Yu, H.-P. Articles by Chaudry, I. H.

Salutary effects of estrogen receptor- agonist on lung injury after trauma-hemorrhage

¹Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama; and ²Graduate Institute of Clinical Medical Sciences, Chang Gung University, Taoyuan, Taiwan

Submitted 2 December 2005 ; accepted in final form 15 December 2005

Although 17-estradiol (E2) administration after trauma-hemorrhage attenuates lung injury in male rodents, it is not known whether the salutary effects are mediated via estrogen receptor (ER)- or ER-. We hypothesized that the salutary effects of E2 lung are mediated via ER-. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure 40 mmHg for 90 min, then resuscitation). E2 (50 µg/kg), ER- agonist propyl pyrazole triol (PPT; 5 µg/kg), ER- agonist diarylpropiolnitrile (DPN; 5 µg/kg), or vehicle (10% DMSO) was injected subcutaneously during resuscitation. At 24 h after trauma-hemorrhage or sham operation, bronchoalveolar fluid (BALF) was collected for protein concentration, LDH activity, and nitrate/nitrite and IL-6 levels. Moreover, lung tissue was used for inducible nitric oxide synthase (iNOS) mRNA/protein expression, nitrate/nitrite and IL-6 levels, and wet/dry weight ratio (n = 6 rats/group). One-way ANOVA and Tukey's test were used for statistical analysis. The results indicated that E2 downregulated lung iNOS expression after trauma-hemorrhage. Protein concentration, LDH activity, and nitrate/nitrite and IL-6 levels in BALF and nitrate/nitrite and IL-6 levels in the lung increased significantly after trauma-hemorrhage; however, administration of DPN but not PPT significantly improved all parameters. Moreover, DPN treatment attenuated trauma-hemorrhage-mediated increase in iNOS mRNA/protein expression in the lung. In contrast, no significant change in the above parameters was observed with PPT. Thus the salutary effects of E2 on attenuation of lung injury are mediated via ER-, and ER--induced downregulation of iNOS likely plays a significant role in the DPN-mediated lung protection after trauma-hemorrhage.

shock; propyl pyrazole triol; diarylpropiolnitrile

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