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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

17 beta-Estradiol protects against lung injuries after brain death in male rats

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Author(s):
Vieira, Roberta Figueiredo [1] ; Breithaupt-Faloppa, Ana Cristina [1] ; Matsubara, Bruno Carvalho [1] ; Rodrigues, Geovana [1] ; Sanches, Marcelo Petrof [1] ; Armstrong-, Jr., Roberto [1] ; Ferreira, Sueli Gomes [1] ; Correia, Cristiano de Jesus [1] ; Moreira, Luiz Felipe P. [1] ; Sannomiya, Paulina [1]
Total Authors: 10
Affiliation:
[1] Univ Sao Paulo, Fac Med, Hosp Clin HCFMUSP, Lab Cirurg Pesquisa Cardiovasc, Inst Coracao, Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: JOURNAL OF HEART AND LUNG TRANSPLANTATION; v. 37, n. 11, p. 1381-1387, NOV 2018.
Web of Science Citations: 1
Abstract

BACKGROUND: Brain death elicits microvascular dysfunction and inflammation, and thereby compromises lung viability for transplantation. As 17 beta-estradiol was shown to be anti-inflammatory and vascular protective, we investigated its effects on lung injury after brain death in male rats. METHODS: Wistar rats were assigned to: sham-operation by trepanation only (SH, n = 7); brain death (BD, n = 7); administration of 17-estradiol (280 tg/kg, iv) at 60 minutes after brain death (BD-E2, n = 7). Experiments were performed 180 minutes thereafter. Histopathological changes in the lung were evaluated by histomorphometry. Gene expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and endothelin-1 was measured by real-time polymerise chain reaction. Protein expression of NO synthases, endothelin-1, platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), BCL-2, and caspase 3 was assessed by immunohistochemistry. Cytokines were quantified by enzyme linked immunosorbent assay. RESULTS: Treatment with 17P-estradiol after brain death decreased lung edema and hemorrhage (p < 0.0001), and serum levels of cytokine-induced neutrophil chemoattractant-1 (CINC-1; p = 0.0020). iNOS (p < 0.0001) and VCAM-1 (p < 0.0001) also diminished at protein levels, while eNOS accumulated (p = 0.0002). However, gene expression of iNOS, eNOS, and endothelin-1 was comparable among groups, as was protein expression of endothelin-1, ICAM-1, BCL-2, and caspase 3. CONCLUSIONS: 17P-Estradiol effectively reduces lung injury in brain-dead rats mainly due to its ability to regulate NO synthases. Thus, the drug may improve lung viability for transplantation. J Heart Lung Transplant 2018;37:1381-1387 (C) 2018 International Society for Heart and Lung Transplantation. All rights reserved. (AU)

FAPESP's process: 16/13632-3 - EVALUATION OF THE EFFECTS OF 17beta-ESTRADIOL ON MICROCIRCULATORY CHANGES INDUCED BY BRAIN DEATH IN MALE RATS
Grantee:Paulina Sannomiya
Support Opportunities: Regular Research Grants