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Am J Physiol Lung Cell Mol Physiol (December 16, 2005). doi:10.1152/ajplung.00504.2005
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Submitted on December 2, 2005
Accepted on December 15, 2005

Salutary Effects of Estrogen Receptor-{beta} Agonist on Lung Injury Following Trauma-Hemorrhage

Huang-Ping Yu1, Ya-Ching Hsieh2, Takao Suzuki2, Tomoharu Shimizu2, Mashkoor A Choudhry2, Martin G Schwacha2, and Irshad H Chaudry2*

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

* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.

Although 17{beta}-estradiol (E2) administration following trauma-hemorrhage attenuates lung injury in male rodents, it is not known whether the salutary effects are mediated via estrogen receptor (ER)-{alpha} or ER-{beta}. We hypothesized that the salutary effects of E2 lung are mediated via ER-{beta}. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean BP 40 mmHg for 90 min, then resuscitation). E2 (50 µ/Kg), ER-{alpha} agonist propyl pyrazole triol (PPT) (5 µg/Kg), ER-{beta} 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 iNOS mRNA/protein expression, nitrate/nitrite, and IL-6 levels, and wet/dry weight ratio (n = 6 rats/group). One-way ANOVA and Tukeys test were used for statistical analysis. The results indicated that E2 downregulated lung iNOS expression following trauma-hemorrhage. Protein concentration, LDH activity, 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-{beta} and ER-{beta}-induced downregulation of iNOS likely plays a significant role in the DPN-mediated lung protection following trauma-hemorrhage.




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