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Title: The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovarieetomized mice
Authors: Oliveira, Flavia de [UNIFESP]
Maifrino, Laura Beatriz Mesiano [UNIFESP]
Jesus, Gustavo Protasio Pacheco de [UNIFESP]
Carvalho, Juliana Goncalves [UNIFESP]
Marchon, Claudia
Ribeiro, Daniel Araki [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Univ Sao Judas Tadeu
Inst Dante Pazzanese Cardiol
Keywords: atherosclerosis
Issue Date: 1-Sep-2013
Publisher: Acad Brasileira De Ciencias
Citation: Anais Da Academia Brasileira De Ciencias. Rio Janeiro: Acad Brasileira De Ciencias, v. 85, n. 3, p. 1157-1164, 2013.
Abstract: Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 (COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice low-density lipoprotein receptor knockout (LDL-KO) with or without ovariectomy. A total of 15 female C57BL/6 mice and 15 female LDE-KO mice were distributed into 6 groups: sedentary control, sedentary control ovariectomized, trained control ovariectomized, LDL-KO sedentary, LDL-KO sedentary ovariectomized and LDL-KO trained ovariectomized. The ascending part of the aorta was stained with H&E and COX-2 expression was assessed by immunohistochemistry. Results revealed that ovariectomy as well as exercise training were not able to induce histopathological changes in mouse aorta for all groups investigated. LDL-KO mice demonstrated plaque containing cholesterol clefts, foamy histiocytes and mild inflammatory process for all groups indistinctly. Ovariectomy induced a strong immunoexpression in atherosclerosis lesion of EDE-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDE-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.
ISSN: 0001-3765
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