A diminuição de estrogênio em mulheres pós-menopausa aumenta o risco de doenças cardiovasculares. Esse risco, como resultado da aterosclerose, pode induzir o processo inflamatório e a expressão da Ciclooxigenase-2 ( COX-2) . O objetivo deste estudo foi investigar a expressão da COX-2 em camundongos fêmeas knockout para o receptor de lipoproteína de baixa densidade ( LDL-KO) submetidas ao exercício com ou sem ovariectomia. Um total de 15 fêmeas C57BL/6 e 15 fêmeas LDL-KO foram divididas em 6 grupos: controle sedentário, controle ovariectomizado sedentário, controle ovariectomizado treinado, LDL-KO sedentário, LDL-KO ovariectomizado sedentário e LDL-KO ovariectomizado treinado. A parte ascendente da aorta foi analisada com H&E e com imunohistoquímica para COX-2. Os resultados revelaram que a ovariectomia bem como o exercício não induziram alterações histopatológicas da aorta dos camundongos em todos os grupos investigados. Camundongos LDL-KO demonstraram placas de ateroma, histiócitos espumosos e processo inflamatório moderado em todos os grupos indistintamente. A ovariectomia induziu a forte imunoexpressão da COX-2 na lesão aterosclerótica dos camundongos LDL-KO. No entanto, foi detectada uma diminuição da expressão da COX-2 no LDL-KO ovariectomizado treinado quando comparado com o LDL-KO sedentário. Nossos dados estão de acordo com a noção de que o exercício pode modular a expressão da COX-2 nos camundongos LDL-KO como resultado da diminuição da expressão da COX-2.

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 LDL-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 LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-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.

OBJECTIVE: The aim of this study was to evaluate overall genetic damage induced by total sleep deprivation in obese, female Zucker rats of differing ages. METHOD: Lean and obese Zucker rats at 3, 6, and 15 months old were randomly distributed into two groups for each age group: home-cage control and sleep-deprived (N = 5/group). The sleep-deprived groups were deprived sleep by gentle handling for 6 hours, whereas the home-cage control group was allowed to remain undisturbed in their home-cage. At the end of the sleep deprivation period, or after an equivalent amount of time for the home-cage control groups, the rats were brought to an adjacent room and decapitated. The blood, brain, and liver tissue were collected and stored individually to evaluate DNA damage. RESULTS: Significant genetic damage was observed only in 15-month-old rats. Genetic damage was present in the liver cells from sleep-deprived obese rats compared with lean rats in the same condition. Sleep deprivation was associated with genetic damage in brain cells regardless of obesity status. DNA damage was observed in the peripheral blood cells regardless of sleep condition or obesity status. CONCLUSION: Taken together, these results suggest that obesity was associated with genetic damage in liver cells, whereas sleep deprivation was associated with DNA damage in brain cells. These results also indicate that there is no synergistic effect of these noxious conditions on the overall level of genetic damage. In addition, the level of DNA damage was significantly higher in 15-month-old rats compared to younger rats.