Abstract
Aging is a predominant risk factor for the development and progression of cardiovascular complications. Physiologically and anatomically, the heart undergoes numerous changes that result in poor cardiac function in the elderly population. Recently, several studies have provided promising results, confirming the ability of the senescence-accelerated mouse-prone 8 (SAMP8) model to accurately model age-related cardiovascular alterations. In this study, using a murine model of senescence, SAMP8, we aimed to investigate the effect of 3,4-dihydroxybenzalacetone (DBL), a catechol-containing phenylpropanoid derivative isolated from Inonotus obliquus (Chaga), on cardiac aging. DBL was administered at the doses of 10 mg/kg and 20 mg/kg by oral gavage to SAMP8 mice to examine aging-mediated cardiac changes, such as oxidative DNA damage, oxygen radical antioxidant capacity (ORAC) value, fibrosis, inflammation, and apoptosis. The treatment with DBL at both doses significantly reduced aging-mediated oxidative DNA damage, and simultaneously increased the ORAC value in the SAMP8 assay. Cardiac fibrosis was assessed with Azan-Mallory staining, and the number of cardiac remodeling markers was found to be significantly reduced after the treatment with DBL. We also observed a decrease in cardiomyocyte apoptosis as measured by the terminal transferase-mediated dUTP nick end labeling (TUNEL) staining method and the caspase-3 levels in SAMP8 mice compared with senescence-resistant control (SAMR1) mice. The findings from this study suggest that DBL has a potentially beneficial effect on aging-mediated myocardial alterations. Further studies are warranted to confirm the promising potential of this catechol compound against aging-associated myocardial dysfunction.
Highlights
Aging is an inevitable, complex biological phenomenon that all living organisms experience.Advancements in health sciences have steadily led to increased longevity, which has significantly increased the elderly population [1]
These data demonstrate that the treatment with DBL increased the oxygen radical antioxidant capacity (ORAC) value in the plasma of senescence-accelerated mouse-prone 8 (SAMP8) mice, and protected against aging-induced free radical generation
Though life expectancy has improved, an increase in longevity enhances the risk of chronic illnesses such
Summary
Complex biological phenomenon that all living organisms experience.Advancements in health sciences have steadily led to increased longevity, which has significantly increased the elderly population [1]. Complex biological phenomenon that all living organisms experience. The myocardium undergoes structural and functional modifications during aging. Cardiac aging is characterized by cellular and molecular alterations in the heart that may include increased mitochondrial oxidative stress, fibrosis, inflammation, and apoptosis [2]. Aging-induced cardiac fibrosis may affect both myocardial relaxation and contractility. The loss of cardiomyocytes through apoptosis is a crucial event underlying the development of cardiac dysfunction, which is evident in the progression of cardiac dysfunction. There is a senescenceinduced inflammation that is sustained through the upregulation of the release of cytokines, leading to the proliferation of fibroblasts an activation of metalloproteinases [3]. Deciphering the molecular mechanisms underlying myocardial dysregulation is important for identifying the targets to potentially intervene and attenuate the degenerative processes in cardiac senescence
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