Cardiac Fas-dependent and mitochondria-dependent apoptosis in ovariectomized rats

Lee, Shin-Da; Kuo, Wei Wen; Ho, Ying-Jui; Lin, Ann Chi; Tsai, Chang Hai; Wang, Hsueh Fang; Kuo, Chia Hua; Yang, Ai Lun; Huang, Chih Yang; Hwang, Jin Ming

doi:10.1016/j.maturitas.2008.07.004

Cited by 48 publications

(50 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The ovariectomy caused myocyte cell apoptosis and/or necrosis without ischemia in the heart tissues of the rats [16,17,18]. In the present study, cardiomyopathic changes, such as abnormal myocardial architecture, inflammatory cell infiltration, edema, increase in fibrosis and the connective tissue component, enlarged interstitial space and widely dispersed cardiac necrotic cells, appeared to be increased in the experimental groups.…”

Section: Discussionsupporting

confidence: 51%

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

et al. 2011

View full text Add to dashboard Cite

Objectives: Menopause has a negative effect on cardiovascular functions. However, very little is known of the overall effect of menopause on the cardiac ultrastructure or the pathophysiological basis of this. Methods: A group of 12-week-old female Sprague Dawley rats were randomly allocated to healthy control (n = 6) and ovariectomy groups (n = 6). Twelve weeks after ovariectomy, the rats’ cardiac tissues were histopathologically analyzed for determination of oxidant and antioxidant enzymes [activities of catalase (CAT), superoxide dismutase (SOD), and myeloperoxidase (MPO) and amount of glutathione (GSH) and lipid peroxidation (LPO)]. Results: When compared to the control group, the ovariectomy group showed cardiomyopathic changes. In tissue, activities of CAT (185 ± 2.4 vs. 112 ± 1.4 mmol/min/mg tissue; p < 0.05), SOD (153 ± 1.0 vs. 146 ± 0.7 mmol/min/mg tissue; p < 0.05) and MPO (19 ± 0.8 vs. 8.6 ± 0.11 µmol/min/mg tissue; p < 0.05) and LPO levels (32.1 ± 0.77 vs. 14.4 ± 0.20 nmol/g tissue; p < 0.05) were significantly increased in the ovariectomy group when compared to the control group. However, GSH levels (3.43 ± 0.02 vs. 3.73 ± 0.01 nmol/g tissue; p < 0.05) were significantly lower in the ovariectomy group when compared to the control group. Conclusion: Using an experimental animal model, we were able to demonstrate that menopause causes cardiomyopathic changes, and we propose that these changes could be mediated by oxidative stress.

show abstract

Section: Discussionsupporting

confidence: 51%

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Furthermore, we also found that appropriate exercise training can enhance the PI3K-Akt pathway (Lee et al 2008;Huang et al 2012;Cheng et al 2013;Lee et al 2013). In FOXO3, the three sites phosphorylated by Akt are Thr32, Ser253, and Ser315.…”

Section: Introductionmentioning

confidence: 58%

“…These data suggest that exercise training, resveratrol treatment, and exercise training combined with resveratrol treatment can all be cardioprotective. Our previous report revealed an antihypertrophic effect in rat hearts from exercise training (Lee et al 2008;Huang et al 2012;Cheng et al 2013;Lee et al 2013). Indeed, the collagen accumulation in the exercise training rat hearts was not as severe as that in the control group (Figs.…”

Section: Discussionmentioning

confidence: 78%

Resveratrol enhanced FOXO3 phosphorylation via synergetic activation of SIRT1 and PI3K/Akt signaling to improve the effects of exercise in elderly rat hearts

Lin

Wei³

et al. 2014

AGE

Self Cite

View full text Add to dashboard Cite

Exercise training is considered a benefit to heart function, but the benefit in aging hearts remains unknown. Activation of the PI3K-Akt survival pathway and suppression of Fas/FADD/caspase-8 apoptotic signaling by exercise training in hearts from young subjects have been described in our previous studies. However, the mechanisms are still unclear and need to be explored in aging hearts. Thus, 18-month-old rats were used as a model and underwent swimming exercise training, resveratrol treatment (15 mg/kg/day), or exercise training with resveratrol treatment for 1 month. The results showed that heart function in each group improved. AGE (2014) 36:9705

show abstract

“…This can be reduced by exercise training. Our previous reports revealed an anti-hypertrophic effect in rat hearts through exercise training (Chang et al 2013;Lee et al 2013;Lee et al 2008;Huang et al 2012). This aging model expression after stimulation is weakened with increasing age.…”

Section: Discussionmentioning

confidence: 95%

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

Lai

Kuo³

et al. 2014

AGE

Self Cite

View full text Add to dashboard Cite

Cardiovascular disease is the second leading cause of death (9.1 %) in Taiwan. Heart function deteriorates with age at a rate of 1 % per year. As society ages, we must study the serious problem of cardiovascular disease. SIRT1 regulates important cellular processes, including anti-apoptosis, neuronal protection, cellular senescence, aging, and longevity. In our previous studies, rats with obesity, high blood pressure, and diabetes exhibiting slowed myocardial performance and induced cell apoptosis were reversed via sports training AGE (2014) 36:9706

show abstract

Cardiac Fas-dependent and mitochondria-dependent apoptosis in ovariectomized rats

Cited by 48 publications

References 37 publications

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

Resveratrol enhanced FOXO3 phosphorylation via synergetic activation of SIRT1 and PI3K/Akt signaling to improve the effects of exercise in elderly rat hearts

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

Contact Info

Product

Resources

About