The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovarieetomized mice

• Autor(a) principal: De Oliveira, Flavia [UNIFESP]
• Data de Publicação: 2013
• Outros Autores: Maifrino, Laura Beatriz Mesiano [UNIFESP], Jesus, Gustavo Protasio Pacheco de [UNIFESP], Carvalho, Juliana Goncalves [UNIFESP], Marchon, Claudia, Ribeiro, Daniel Araki [UNIFESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: https://dx.doi.org/10.1590/S0001-37652013005000046; https://repositorio.unifesp.br/handle/11600/42529
• topic: Atherosclerosis; Ciclooxygenase-2; Exercise; Menopause

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.